Vedci varuj\u00fa, \u017ee bakt\u00e9rie si vedia odovzd\u00e1va\u0165 g\u00e9ny pre tox\u00edny<\/strong> a rezistenciu na antibiotik\u00e1<\/strong> \u2013 a to neuverite\u013ene r\u00fdchlo!<\/p>\n\n\n\n V\u00e4\u010d\u0161ina g\u00e9nov bakt\u00e9rie je „uzamknut\u00e1“ v jej hlavnej DNA. Ale g\u00e9ny, ktor\u00e9 k\u00f3duj\u00fa tox\u00edny alebo odolnos\u0165 vo\u010di liekom, s\u00fa \u010dasto naviazan\u00e9 na \u0161peci\u00e1lne bal\u00ed\u010dky, ktor\u00e9 naz\u00fdvame Mobiln\u00e9 Genetick\u00e9 Elementy (MGEs)<\/strong>.<\/p>\n\n\n\n Tieto MGEs s\u00fa ako genetick\u00ed kuri\u00e9ri<\/strong> alebo ako mal\u00e9 USB k\u013e\u00fa\u010de. Umo\u017e\u0148uj\u00fa bakt\u00e9ri\u00e1m r\u00fdchlo si navz\u00e1jom „posla\u0165“ kritick\u00e9 inform\u00e1cie. Deje sa to procesom, ktor\u00fd sa vol\u00e1 Horizont\u00e1lny Prenos G\u00e9nov (HGT)<\/strong>, a ten men\u00ed pravidl\u00e1 hry:<\/p>\n\n\n\n Vedci v \u010dl\u00e1nku detailne opisuj\u00fa, ako si Salmonella<\/em>, Clostridium difficile<\/em> (zn\u00e1my vinn\u00edk nemocni\u010dn\u00fdch hna\u010diek) a in\u00e9 \u010drevn\u00e9 patog\u00e9ny vymie\u0148aj\u00fa toxick\u00e9 g\u00e9ny, ktor\u00e9 sp\u00fa\u0161\u0165aj\u00fa ochorenia.<\/p>\n\n\n\n Ide o neust\u00e1le prebiehaj\u00facu genetick\u00fa v\u00fdzbroj<\/strong> vo va\u0161om \u010dreve, kde je tox\u00edn, ktor\u00fd dnes produkuje jeden patog\u00e9n, zajtra u\u017e s\u00fa\u010das\u0165ou arzen\u00e1lu inej bakt\u00e9rie.<\/p>\n\n\n\n Z\u00e1ver:<\/strong> Zdrav\u00fd mikrobi\u00f3m nie je len o dobrom tr\u00e1ven\u00ed. Je to va\u0161a prv\u00e1 l\u00ednia obrany<\/strong>, ktor\u00e1 rozhoduje o tom, ktor\u00e9 bakt\u00e9rie si vedia vo va\u0161om \u010dreve po\u017ei\u010da\u0165 a odovzda\u0165 najnebezpe\u010dnej\u0161ie genetick\u00e9 k\u00f3dy.<\/p>\n\n\n\n Slovensk\u00fa verziu \u010dl\u00e1nku n\u00e1jdete ni\u017e\u0161ie. N\u00e1zov \u010dl\u00e1nku v sloven\u010dine je: Mobiln\u00e9 genetick\u00e9 prvky spojen\u00e9 s tox\u00ednmi v hlavn\u00fdch \u010drevn\u00fdch bakteri\u00e1lnych patog\u00e9noch<\/strong><\/p>\n\n\n\n Shruti Panwar, Shashi Kumari, Jyoti Verma, Susmita Bakshi, Lekshmi Narendrakumar,Deepjyoti Paul and Bhabatosh Das* Abstrakt <\/em><\/strong><\/p>\n\n\n\n Jedn\u00fdm z fascinuj\u00facich v\u00fdsledkov \u0161t\u00fadi\u00ed \u013eudsk\u00e9ho mikrobi\u00f3mu vyu\u017e\u00edvaj\u00facich multi-omick\u00fa technol\u00f3giu je schopnos\u0165 de\u0161ifrova\u0165 mili\u00f3ny mikrobi\u00e1lne k\u00f3dovan\u00fdch funkci\u00ed v najkomplexnej\u0161om a najhustej\u0161ie os\u00eddlenom mikrobi\u00e1lnom ekosyst\u00e9me, vr\u00e1tane \u013eudsk\u00e9ho gastrointestin\u00e1lneho traktu (GI), bez kultiv\u00e1cie mikr\u00f3bov. Je dobre zn\u00e1me, \u017ee viacer\u00e9 funkcie, ktor\u00e9 moduluj\u00fa \u013eudsk\u00fd metabolizmus, asimil\u00e1ciu \u017eiv\u00edn, imunitu, infekcie, z\u00e1va\u017enos\u0165 ochoren\u00ed a terapeutick\u00fa \u00fa\u010dinnos\u0165 liekov, maj\u00fa preva\u017ene mikrobi\u00e1lny p\u00f4vod. Okrem toho s\u00fa tieto mikrobi\u00e1lne funkcie dynamick\u00e9 a m\u00f4\u017eu sa \u0161\u00edri\u0165 medzi mikrobi\u00e1lnymi tax\u00f3nmi \u017eij\u00facimi v rovnakom ekosyst\u00e9me alebo in\u00fdch mikrobi\u00e1lnych ekosyst\u00e9moch prostredn\u00edctvom horizont\u00e1lneho prenosu g\u00e9nov. Pre klinick\u00fdch lek\u00e1rov aj v\u00fdskumn\u00edkov je mimoriadne d\u00f4le\u017eit\u00e9 pochopi\u0165 tox\u00edny, faktory virulence a vlastnosti rezistencie vo\u010di liekom k\u00f3dovan\u00e9 mikr\u00f3bmi spojen\u00fdmi s \u013eudsk\u00fdm telom. Ke\u010f s\u00fa v\u0161ak tak\u00e9to vlastnosti geneticky spojen\u00e9 s mobiln\u00fdmi genetick\u00fdmi prvkami (MGE), ktor\u00e9 ich robia prenosn\u00fdmi, vytv\u00e1ra to dodato\u010dn\u00fa z\u00e1\u0165a\u017e pre verejn\u00e9 zdravie. T\u00e1to \u0161t\u00fadia sa zameriava hlavne na funkcie komenz\u00e1lov v \u010dreve a dynamiku a vz\u00e1jomn\u00e9 p\u00f4sobenie medzi komenz\u00e1lnymi a patog\u00e9nnymi bakt\u00e9riami v \u010dreve. \u0160t\u00fadia tie\u017e sumarizuje mno\u017estvo MGE spojen\u00fdch s virulentn\u00fdmi g\u00e9nmi pr\u00edtomn\u00fdmi v gen\u00f3moch r\u00f4znych enterick\u00fdch bakteri\u00e1lnych patog\u00e9nov, ktor\u00e9 s\u00fa prenosn\u00e9 medzi in\u00fdmi patog\u00e9nmi a komenz\u00e1lmi.<\/p>\n\n\n\n K\u013e\u00fa\u010dov\u00e9 slov\u00e1: Mobiln\u00e9 genetick\u00e9 prvky; mikrobi\u00f3m; patog\u00e9ny; tox\u00edny; horizont\u00e1lny prenos g\u00e9nov; rezistencia na lieky<\/p>\n\n\n\n \u00davod <\/em><\/strong><\/p>\n\n\n\n Term\u00edn \u201e\u010drevn\u00e1 mikrobiota\u201c ozna\u010duje cel\u00fa popul\u00e1ciu mikroorganizmov, ktor\u00e9 \u017eij\u00fa v \u013eudskom \u010dreve, a zah\u0155\u0148a bakt\u00e9rie, huby, archey, prvoky a v\u00edrusy (Sekirovetal., 2010). Bakteri\u00e1lna mikrobiota \u010dloveka bola d\u00f4kladne presk\u00faman\u00e1, ale v\u00fdskum ostatn\u00fdch r\u00ed\u0161 je st\u00e1le v po\u010diato\u010dnom \u0161t\u00e1diu. Preh\u013ead r\u00f4znorod\u00fdch zlo\u017eiek mikrobioty \u013eudsk\u00e9ho \u010dreva je uveden\u00fd na obr\u00e1zku 1 spolu s jej hlavn\u00fdmi zlo\u017ekami. \u010crevo m\u00e1 ve\u013ek\u00fd pr\u00edsun mikronutrientov, \u0161irok\u00fd rozsah pH a pr\u00edstup k kysl\u00edku, vod\u00edku a met\u00e1nu, \u010do z neho rob\u00ed preferovan\u00e9 miesto pre mikrobi\u00e1lnu koloniz\u00e1ciu a vhodn\u00e9 prostredie pre horizont\u00e1lny prenos g\u00e9nov (HGT) (Kurokawa et al., 2007). Za posledn\u00fdch 10 rokov viacero \u0161t\u00fadi\u00ed pouk\u00e1zalo na interakcie medzi bakt\u00e9riami a ich hostite\u013emi. V \u013eudskom \u010dreve m\u00f4\u017eu by\u0165 bakt\u00e9rie komenz\u00e1lne, symbiotick\u00e9, patobiontn\u00e9 alebo patog\u00e9nne (Matija\u0161i\u0107 et al., 2020). Komens\u00e1lne bakt\u00e9rie v \u010dreve hraj\u00fa d\u00f4le\u017eit\u00fa \u00falohu pri produkcii vitam\u00ednov, synt\u00e9ze mastn\u00fdch kysel\u00edn s kr\u00e1tkym re\u0165azcom (SCFA), regul\u00e1cii bari\u00e9rovej funkcie, imunomodul\u00e1cii a mnoh\u00fdch \u010fal\u0161\u00edch procesoch, \u010d\u00edm podporuj\u00fa homeost\u00e1zu organizmu (Valdes et al., 2018). Je zn\u00e1me, \u017ee inhibuj\u00fa rast patog\u00e9nnych bakt\u00e9ri\u00ed prostredn\u00edctvom procesu zn\u00e1meho ako \u201erezistencia na koloniz\u00e1ciu\u201c, bu\u010f produkciou metabolitov, ktor\u00e9 inhibuj\u00fa rast patog\u00e9nov, alebo regul\u00e1ciou imunitn\u00e9ho syst\u00e9mu hostite\u013ea. Existuje v\u0161ak aj nieko\u013eko spr\u00e1v, ktor\u00e9 nazna\u010duj\u00fa, \u017ee komenz\u00e1ly m\u00f4\u017eu pom\u00e1ha\u0165 koloniz\u00e1cii patog\u00e9nov t\u00fdm, \u017ee vylu\u010duj\u00fa \u017eiviny, ktor\u00e9 tieto bakt\u00e9rie \u017eivia, \u010do im umo\u017e\u0148uje nakoniec prekona\u0165 komenz\u00e1ly a sp\u00f4sobi\u0165 ochorenie (Rolhion a Chassaing, 2016). Okrem toho predch\u00e1dzaj\u00face v\u00fdskumy uk\u00e1zali, \u017ee komenz\u00e1ly produkuj\u00fa mal\u00e9 zl\u00fa\u010deniny z muk\u00f3znej vrstvy hostite\u013ea, ktor\u00e9 moduluj\u00fa virulenciu enterohemoragick\u00e9ho Escherichia coli (Jubelin et al., 2018). Je dobre zdokumentovan\u00e9, \u017ee patog\u00e9nne mikroorganizmy maj\u00fa schopnos\u0165 vymie\u0148a\u0165 si g\u00e9ny s nepatog\u00e9nnymi obyvate\u013emi \u010driev (Messerer et al., 2017). Aby sme pochopili, ako sa infekcie vyv\u00edjaj\u00fa v \u010dreve, mus\u00edme d\u00f4kladne pozna\u0165 ekol\u00f3giu a genetick\u00e9 charakteristiky mnoh\u00fdch bakt\u00e9ri\u00ed, ktor\u00e9 prevl\u00e1daj\u00fa v \u013eudskom \u010dreve. V\u00fdvoj met\u00f3d a technol\u00f3gi\u00ed za posledn\u00fdch 20 rokov, najm\u00e4 zavedenie sekvenovania novej gener\u00e1cie, zlep\u0161il na\u0161u schopnos\u0165 pochopi\u0165 a sk\u00fama\u0165 pr\u00ednos \u010dlenov mikrobioty a ich \u00falohu v \u013eudskom zdrav\u00ed. Bakteri\u00e1lny gen\u00f3m sa del\u00ed na dve \u0161irok\u00e9 kateg\u00f3rie, a to jadrov\u00fd a doplnkov\u00fd gen\u00f3m. Pr\u00eddavn\u00fd gen\u00f3m je rast\u00faci genov\u00fd fond s neesenci\u00e1lnymi schopnos\u0165ami, ktor\u00e9 poskytuj\u00fa v\u00fdhodu pre pre\u017eitie v danej nika, zatia\u013e \u010do jadrov\u00fd gen\u00f3m k\u00f3duje prote\u00edny, ktor\u00e9 s\u00fa potrebn\u00e9 pre metabolick\u00e9 funkcie (Rankinet al., 2011). G\u00e9ny odoln\u00e9 vo\u010di antibiotik\u00e1m (Acman et al., 2022) a g\u00e9ny virulencie (Juhas et al., 2015) patria medzi genov\u00e9 fondy nach\u00e1dzaj\u00face sa v doplnkovom gen\u00f3me a \u0161\u00edria sa najm\u00e4 horizont\u00e1lnymi transferov\u00fdmi procesmi (Brito et al., 2016), t. j. transdukciou, konjug\u00e1ciou, prirodzenou transform\u00e1ciou a f\u00faziou vezik\u00fal vonkaj\u0161ej membr\u00e1ny (obr\u00e1zok 2). V porovnan\u00ed s jadrov\u00fdm gen\u00f3mom je exog\u00e9nna DNA \u013eahko rozl\u00ed\u0161ite\u013en\u00e1 v\u010faka svojmu jedine\u010dn\u00e9mu zlo\u017eeniu G \u00fe C a \u0161pecifick\u00fdm miestam vlo\u017eenia (Ochman et al., 2000). Mobiln\u00e9 genetick\u00e9 elementy (MGE) s\u00fa jedn\u00fdm z hlavn\u00fdch facilit\u00e1torov HGT (Gyles a Boerlin, 2013). MGE zah\u0155\u0148aj\u00fa prof\u00e1gy, kompozitn\u00e9 transpoz\u00f3ny, patog\u00e9nne ostrovy, f\u00e1gy, integra\u010dn\u00e9 konjuga\u010dn\u00e9 elementy (ICE), plazmidy at\u010f. (Davis a Waldor, 2002). Prenos MGE v \u010dreve vedie k prenosu nielen g\u00e9nov rezistencie vo\u010di antibiotik\u00e1m (ARG), ale aj g\u00e9nov, ktor\u00e9 k\u00f3duj\u00fa metabolick\u00e9 kompetencie, ako je detoxik\u00e1cia so\u013eou, vyu\u017eitie polysacharidov a degrad\u00e1cia hlienu (Broaders et al., 2013). Bohatos\u0165 a rozmanitos\u0165 t\u00fdchto MGE v \u013eudskom \u010dreve s\u0165a\u017euje \u00fapln\u00e9 pochopenie ich ekologick\u00fdch a biologick\u00fdch ident\u00edt. Mnoho publikovan\u00fdch \u010dl\u00e1nkov u\u017e potvrdilo, \u017ee MGE sa z\u00edskavaj\u00fa prostredn\u00edctvom HGT a s\u00fa spojen\u00e9 s g\u00e9nmi k\u00f3duj\u00facimi rezistenciu vo\u010di antibiotik\u00e1m (Kent et al., 2020;<\/p>\n\n\n\n von Wintersdorff et al., 2016; Wang et al., 2022), ale MGE spojen\u00e9 s g\u00e9nmi virulencie s\u00fa menej zd\u00f4raz\u0148ovan\u00e9 (Partridge et al., 2018). Mnoh\u00e9 bakteri\u00e1lne chromoz\u00f3my a mobiln\u00e9 genetick\u00e9 komponenty maj\u00fa syst\u00e9my tox\u00edn-antitox\u00edn (TA) (Peltier et al., 2020; Schmidt a Hensel, 2004; Weaver et al., 2017). Komens\u00e1ly zvy\u010dajne nemaj\u00fa virulentn\u00e9 vlastnosti a akt\u00edvne produkuj\u00fa l\u00e1tky, ktor\u00e9 podporuj\u00fa stabiln\u00e9 interakcie s in\u00fdmi bakt\u00e9riami, ktor\u00e9 zabra\u0148uj\u00fa ich vstupu do potenci\u00e1lne \u0161kodliv\u00fdch ciest. Zmeny v ekol\u00f3gii, ktor\u00e9 vytv\u00e1raj\u00fa nov\u00e9 biotopy, alebo prenos g\u00e9nov virulencie z patog\u00e9nov ved\u00fa k transform\u00e1cii komenz\u00e1lov na patog\u00e9ny. Nadobudnutie tox\u00ednov alebo g\u00e9nov spojen\u00fdch s chorobami, ako s\u00fa patog\u00e9nne ostrovy, s\u00fa pr\u00edkladmi mechanizmov, ktor\u00e9 prispievaj\u00fa k transform\u00e1cii komenz\u00e1lov na patog\u00e9ny a destabiliz\u00e1cii interakcie medzi komenz\u00e1lmi a hostite\u013eom (Gilmore et al., 2013). Alternat\u00edvne m\u00f4\u017ee strata komenz\u00e1lnych funkci\u00ed vies\u0165 k virulencii, ako sa zd\u00e1, \u017ee sa stalo v pr\u00edpadoch Yersinia pestis (Chain et al., 2004) a Bordetella pertussis (Parkhill et al., 2003). T\u00e1to \u0161t\u00fadia sumarizuje r\u00f4zne MGE pr\u00edtomn\u00e9 v gen\u00f3moch enterick\u00fdch patog\u00e9nov a in\u00fdch komenz\u00e1lnych bakt\u00e9ri\u00ed pr\u00edtomn\u00fdch v \u010dreve a ich \u00falohu v produkcii tox\u00ednov, patogen\u00e9ze a v\u00fdvoji ochoren\u00ed. T\u00e1to komplexn\u00e1 \u0161t\u00fadia objas\u0148uje \u00falohu MGE pri formovan\u00ed ekol\u00f3gie a evol\u00facie \u010drevn\u00e9ho mikrobi\u00f3mu a ako ved\u00fa k adapt\u00e1cii komunity na \u010drevn\u00e9 prostredie.<\/p>\n\n\n\n Dynamick\u00fd mikrobi\u00f3m \u013eudsk\u00e9ho \u010dreva<\/em><\/strong> <\/p>\n\n\n\n \u013dudsk\u00e9 \u010drevo je domovom komplexnej a dynamickej mikrobi\u00e1lnej komunity. Zlo\u017eenie \u010drevnej mikrobioty ovplyv\u0148uje \u0161irok\u00e1 \u0161k\u00e1la premenn\u00fdch, vr\u00e1tane sp\u00f4sobu p\u00f4rodu (Reyman et al., 2019), stravy (David et al., 2014; Muegge et al., 2011), \u017eivotn\u00e9ho \u0161t\u00fdlu a genetiky hostite\u013ea (Qin et al., 2022). Na mikrobi\u00f3m \u010dreva vpl\u00fdvaj\u00fa evolu\u010dn\u00e9 dynamick\u00e9 procesy, ako s\u00fa mut\u00e1cie, horizont\u00e1lny g\u00e9nov\u00fd prenos, drift a selekcia, ako aj ekologick\u00e9 faktory, ako s\u00fa zmeny v abundancii druhov alebo nahradenie kme\u0148ov (Garud a Pollard 2020). Av\u0161ak aj dnes existuj\u00fa ve\u013ek\u00e9 medzery v na\u0161ich poznatkoch o glob\u00e1lnej variabilite mikrobi\u00f3mu. Bolo zisten\u00e9, \u017ee industrializ\u00e1cia, westerniz\u00e1cia a rozdiely medzi vidiekom a mestom v r\u00e1mci jednej krajiny s\u00fa hlavn\u00fdmi pr\u00ed\u010dinami tejto heterogenity (De Filipo et al., 2017). Environment\u00e1lne faktory, genetika, strava, choroby a vystavenie antibiotik\u00e1m zohr\u00e1vaj\u00fa v\u00fdznamn\u00fa \u00falohu pri ur\u010dovan\u00ed diverzity a zlo\u017eenia mikroorganizmov v r\u00f4znych \u010dastiach tela. Rozmanit\u00e1 \u0161k\u00e1la faktorov, ktor\u00e9 m\u00f4\u017eu ovplyv\u0148ova\u0165 homeost\u00e1zu \u010driev a mikrobi\u00e1lnu diverzitu, je zn\u00e1zornen\u00e1 na obr\u00e1zku 3. P\u00e4\u0165 hlavn\u00fdch kme\u0148ov \u010drevn\u00fdch bakt\u00e9ri\u00ed s\u00fa Firmicutes, Bacteroidetes, Actinobacteria, Proteobacteria, Fusobacteria a Verrucomicrobia, pri\u010dom Firmicutes a Bacteroidetes tvoria 90 % \u010drevnej mikrobioty zdrav\u00e9ho \u010dloveka (Arumugam et al., 2011). Kme\u0148 Firmicutes sa sklad\u00e1 z viac ako 200 r\u00f4znych rodov, ktor\u00e9 tvoria Lactobacillus, Bacillus, Clostridium, Enterococcus a Ruminococcus. Rod Clostridium predstavuje 95 % kme\u0148a Firmicutes. Bacteroidetes sa sklad\u00e1 z prevl\u00e1daj\u00facich rodov, ako s\u00fa Bacteroides a Prevotella. Kme\u0148 Actinobacteria je proporcion\u00e1lne menej zast\u00fapen\u00fd a reprezentuje ho hlavne rod Bifidobacterium. Hlavn\u00fdmi \u010drevn\u00fdmi patog\u00e9nmi s\u00fa Bacteroides fragilis, Clostridium perfringens, Clostridium botulinum, C. difficile, Enterococcus faecalis, Staphylococcus aureus, Salmonella sp., Shigella sp., Vibrio parahaemolyticus, V. cholerae, Yersinia sp. a Helicobacter pylori patriace do kme\u0148ov Bacteroidetes, Firmicutes a Proteobacteria. \u010crevn\u00e1 mikrobiota sa tie\u017e l\u00ed\u0161i v z\u00e1vislosti od anatomick\u00fdch oblast\u00ed \u010dreva, ktor\u00e9 maj\u00fa tie\u017e odli\u0161n\u00e9 fyziologick\u00e9 charakteristiky, pH a nap\u00e4tie kysl\u00edka, hojnos\u0165 substr\u00e1tu a sekr\u00e9ciu hostite\u013ea (Zhang et al., 2015). Vzh\u013eadom na dynamick\u00fa povahu \u010drevnej mikrobi\u00f3my existuj\u00fa v\u00fdznamn\u00e9 rozdiely v zlo\u017een\u00ed a diverzite \u010drevnej mikrobi\u00f3my medzi \u013eu\u010fmi r\u00f4znych n\u00e1rodov. Niektor\u00e9 bakt\u00e9rie s\u00fa \u0161pecifick\u00e9 pre \u013eud\u00ed z ur\u010ditej geografickej oblasti. Okrem toho boli identifikovan\u00e9 aj \u0161pecifick\u00e9 g\u00e9ny bakt\u00e9ri\u00ed, ktor\u00e9 sa vyskytuj\u00fa v\u00fdlu\u010dne u \u013eud\u00ed z ur\u010ditej geografickej oblasti alebo etnickej skupiny. Pod\u013ea v\u00fdskumu, ktor\u00fd vykonali Chen a kolegovia (Chen et al., 2020), bola vy\u0161\u0161ia hojnos\u0165 g\u00e9nu ppsA pozorovan\u00e1 iba u Pseudomonas tutzerio eur\u00f3pskej popul\u00e1cie. \u010ealej je zn\u00e1me, \u017ee Burkholderia pseudomallei S13 je roz\u0161\u00edrenej\u0161ia v eur\u00f3pskej popul\u00e1cii. Okrem toho sa zistilo, \u017ee prevalencia Bacteroides je vy\u0161\u0161ia v eur\u00f3pskej a americkej popul\u00e1cii ako v \u00e1zijskej, a g\u00e9n MH0053_GL0075770 bol spojen\u00fd s metabolizmom tukov a mohol by s\u00favisie\u0165 s vysokotu\u010dnou stravou eur\u00f3pskej a americkej popul\u00e1cie (Chen et al., 2016). Okrem toho v\u00fdskumy uk\u00e1zali, \u017ee Prevotella a Treponema s\u00fa \u010dastej\u0161ie u \u013eud\u00ed v Burkina Faso, africkej krajine, ktorej obyvatelia pr\u00edsne dodr\u017eiavaj\u00fa vegetari\u00e1nsku stravu (De Filippo et al., 2010). Zauj\u00edmav\u00e9 je, \u017ee u det\u00ed v Japonsku bol identifikovan\u00fd jedine\u010dn\u00fd mikrobi\u00f3m s vysok\u00fdm v\u00fdskytom Bifidobacteriaceae a n\u00edzkym v\u00fdskytom Enterobacteriaceae, \u010do poukazuje na vysoko hygienick\u00fd \u017eivotn\u00fd \u0161t\u00fdl japonskej popul\u00e1cie a jej stravovacie n\u00e1vyky (Nakayama et al., 2015). Prevalencia Bacteroides plebeius v \u010drevnom mikrobi\u00f3me japonskej popul\u00e1cie, ktor\u00fd dok\u00e1\u017ee metabolizova\u0165 porfyr\u00e1n pr\u00edtomn\u00fd v morsk\u00fdch riasach, potvrdzuje s\u00favislos\u0165 medzi stravou a mikrobi\u00f3mom GI (Hehemann et al., 2010). Pod\u013ea Das et al. (2018) dominuj\u00fa v \u010drevnom mikrobi\u00f3me indick\u00fdch komun\u00edt Firmicutes, Bacteroidetes, Actinobacteria a Proteobacteria. Prevotella a Candida boli u Indov \u010dastej\u0161ie ako u Japoncov kv\u00f4li rastlinnej strave indickej popul\u00e1cie (Pareek et al., 2019). \u010eal\u0161ia zauj\u00edmav\u00e1 \u0161t\u00fadia Rothschild et al. (2018) podporuje my\u0161lienku, \u017ee environment\u00e1lne faktory dominuj\u00fa pri formovan\u00ed \u010drevn\u00e9ho mikrobi\u00f3mu. Individu\u00e1lne polymorfizmy jedn\u00e9ho nukleotidu (SNP) alebo genetick\u00fd p\u00f4vod nemaj\u00fa v\u00fdznamn\u00fd vplyv na mikrobiotu a predt\u00fdm hl\u00e1sen\u00e9 vz\u0165ahy nie s\u00fa konzistentne pozorovan\u00e9 vo v\u0161etk\u00fdch \u0161t\u00fadi\u00e1ch (). Hoci sa environment\u00e1lne vplyvy pova\u017euj\u00fa za hlavn\u00fd faktor ovplyv\u0148uj\u00faci v\u00fdvoj \u010drevn\u00e9ho mikrobi\u00f3mu, individu\u00e1lna genetika tie\u017e zohr\u00e1va \u00falohu v zlo\u017een\u00ed mikrobi\u00f3mu (Jakobsson et al., 2010). Nieko\u013eko celogen\u00f3mov\u00fdch asocia\u010dn\u00fdch \u0161t\u00fadi\u00ed spojilo genetick\u00e9 vari\u00e1cie hostite\u013ea v imunitn\u00fdch dr\u00e1hach so zlo\u017een\u00edm mikrobi\u00f3mu v zdravom a chorom stave (Blekhman et al., 2015). Zistilo sa, \u017ee mut\u00e1cie v g\u00e9ne stredomorskej hor\u00fa\u010dky (MEFV) s\u00fa spojen\u00e9 so zmenami v \u0161trukt\u00fare \u010drevnej mikrobi\u00f3movej komunity (Khachatryan et al., 2008). R\u00f4zne genetick\u00e9 faktory hostite\u013ea a imunitn\u00e9 faktory hostite\u013ea, ktor\u00e9 maj\u00fa \u00falohu pri formovan\u00ed \u013eudsk\u00e9ho mikrobi\u00f3mu, s\u00fa uveden\u00e9 v datab\u00e1ze \u201eHost Genetic and Immune factors shaping human Microbiota (GIMICA)\u201c (Tang et al., 2021). Okrem toho, rozdielna expoz\u00edcia r\u00f4znym antibiotik\u00e1m tie\u017e men\u00ed mikrobi\u00e1lny profil \u010dloveka. Observovan\u00e9 \u0161t\u00fadie zistili negat\u00edvny vz\u0165ah medzi prevalenciou mikrobi\u00e1lnych komun\u00edt a expoz\u00edciou antibiotik\u00e1m (Korpela et al., 2016). Zauj\u00edmav\u00e9 je, \u017ee aj lieky, ktor\u00e9 nie s\u00fa antibiotikami, ako napr\u00edklad metform\u00edn pou\u017e\u00edvan\u00fd hlavne na lie\u010dbu cukrovky 2. typu, boli identifikovan\u00e9 ako pr\u00ed\u010dina dysbi\u00f3zy komenz\u00e1lnych bakt\u00e9ri\u00ed v \u010dreve (Forslund et al., 2015). V recenzii sa rozoberaj\u00fa funkcie komenz\u00e1lnych bakt\u00e9ri\u00ed v \u010dreve, hlavn\u00e9 \u010drevn\u00e9 patog\u00e9ny a dynamika MGE medzi komenz\u00e1lmi a patog\u00e9nmi, ktor\u00e9 s\u00fa d\u00f4le\u017eit\u00e9 pre homeost\u00e1zu \u010dreva a progresiu ochorenia.<\/p>\n\n\n\n Funkcie komenz\u00e1lnych bakt\u00e9ri\u00ed v \u010dreve <\/em><\/strong><\/p>\n\n\n\n Je zn\u00e1me, \u017ee pr\u00edtomnos\u0165 komenz\u00e1lnych bakt\u00e9ri\u00ed v \u010dreve udr\u017eiava homeost\u00e1zu \u010dreva a m\u00e1 v\u00fdznamn\u00fd vplyv na zdravie a choroby \u010dloveka. Anal\u00fdza 1520 kultivovate\u013en\u00fdch referen\u010dn\u00fdch gen\u00f3mov komenz\u00e1lnych bakt\u00e9ri\u00ed, vykonan\u00e1 v r\u00e1mci Kyoto Encyclopedia of Genes and Genomes (Kanehisa a Goto, 2000), odhalila, \u017ee sa vo v\u00e4\u010d\u0161ej miere podie\u013eaj\u00fa na metabolizme sacharidov a aminokysel\u00edn (Zou et al., 2019). Bolo zisten\u00e9, \u017ee kmene Fusobacteria, Bacteroidetes, Proteobacteria a in\u00e9 gramnegat\u00edvne bakt\u00e9rie disponuj\u00fa \u0161irokou \u0161k\u00e1lou g\u00e9nov biosynt\u00e9zy lipopolysacharidov (ko00540). G\u00e9ny, ktor\u00e9 funguj\u00fa v smere degrad\u00e1cie glyk\u00e1nov (ko00531 a ko00511), boli identifikovan\u00e9 ako hojn\u00e9 v Bacter oidetes, \u010do nazna\u010duje ich \u00fa\u010das\u0165 na katabolizme sacharidov. \u010ealej boli identifikovan\u00e9 g\u00e9ny podie\u013eaj\u00face sa na metabolizme sfingolipidov (ko00600) a synt\u00e9ze steroidn\u00fdch horm\u00f3nov (ko00140), ktor\u00e9 s\u00fa hojn\u00e9 v Bacteroidetes. Proteobacteria boli identifikovan\u00e9 ako bohat\u00e9 na g\u00e9ny podie\u013eaj\u00face sa na degrad\u00e1cii xenobiot\u00edk (ko01220) (Zou et al., 2019). Mnoho virulentn\u00fdch faktorov a ARG bolo v\u0161ak tie\u017e zmapovan\u00fdch v datab\u00e1ze virulentn\u00fdch faktorov (Chen et al., 2005) a komplexnej datab\u00e1ze antibiotickej rezistencie (Alcock et al., 2020) v bakt\u00e9ri\u00e1ch patriacich do kme\u0148a Proteobacteria, \u010do nazna\u010duje ich schopnos\u0165 sp\u00f4sobi\u0165 ochorenia. Esenci\u00e1lne koenz\u00fdmy, ako je kobalam\u00edn, zachyt\u00e1vaj\u00fa komenz\u00e1ly v \u010dreve pomocou lipoprote\u00ednov vystaven\u00fdch na povrchu (Wexler et al., 2018). Biosynt\u00e9za queuos\u00ednu, n\u00e1hrady guan\u00ednu, ktor\u00e1 m\u00e1 v\u00fdznam pri mnoh\u00fdch fyziologick\u00fdch poruch\u00e1ch, ako je progresia rakoviny, neurologick\u00e9 deformity a zv\u00fd\u0161en\u00e1 prolifer\u00e1cia buniek, bola identifikovan\u00e1 ako proces vykon\u00e1van\u00fd E. coli a Bacillus subtilis. Toto bolo potvrden\u00e9 \u0161t\u00fadiom mutanta g\u00e9nu biosynt\u00e9zy queuos\u00ednu E. coli, ktor\u00fd akumuloval epoxyqueuos\u00edn (Miles et al., 2011). Hlavn\u00fdmi produktmi sacharolytick\u00e9ho kvasenia sacharidov, zn\u00e1mymi ako SCFA, s\u00fa mrav\u010dan, acet\u00e1t, propion\u00e1t a butyr\u00e1t, ktor\u00e9 maj\u00fa r\u00f4zne funkcie pri udr\u017eiavan\u00ed zdravej fyziol\u00f3gie \u010driev, vr\u00e1tane integrity bari\u00e9ry, imunomodul\u00e1cie, prolifer\u00e1cie epitelu a regul\u00e1cie chuti do jedla (Chambers et al., 2014; Magne et al., 2020; Morrison a Preston, 2016). Je zn\u00e1me, \u017ee \u010drevn\u00e9 komenz\u00e1ly rozkladaj\u00fa vl\u00e1kninu z potravy, \u010d\u00edm uvo\u013e\u0148uj\u00fa deriv\u00e1ty indolu, ktor\u00e9 aktivuj\u00fa AhR (arylhydrokarb\u00f3nov\u00fd receptor) a iniciuj\u00fa ILC3 (vroden\u00e9 lymfoidn\u00e9 bunky typu 3) bunky, aby posilnili \u010drevn\u00fa sliznicu prostredn\u00edctvom interleuk\u00ednu-22 (Postler a Ghosh, 2017). \u010ealej, komenz\u00e1lne bakt\u00e9rie v \u010dreve metabolizuj\u00fa argin\u00edn, aby vylu\u010dovali polyam\u00edny, ktor\u00e9 inhibuj\u00fa inflamat\u00f3zny komplex NLRP6 (NOD-podobn\u00fd receptor obsahuj\u00faci pyr\u00ednov\u00fa dom\u00e9nu 6) a tie\u017e zmier\u0148uj\u00fa proz\u00e1palov\u00e9 cytok\u00edny (Levy et al., 2015). Metabolity \u010drevn\u00e9ho mikrobi\u00f3mu s\u00fa tie\u017e zn\u00e1me t\u00fdm, \u017ee inhibuj\u00fa synt\u00e9zu proz\u00e1palov\u00fdch g\u00e9nov z\u00e1visl\u00fa od jadrov\u00e9ho faktora \u03baB, ktor\u00fd moduluje cytok\u00edny (Zhang et al., 2022). Okrem toho je zn\u00e1me, \u017ee \u010drevn\u00e9 bakt\u00e9rie m\u00f4\u017eu meni\u0165 \u017el\u010dov\u00e9 soli generovan\u00e9 hostite\u013eom, ktor\u00e9 s\u00fa d\u00f4le\u017eit\u00e9 pre signaliz\u00e1ciu a zv\u00fd\u0161enie funkcie epitelovej bari\u00e9ry (Sayin et al., 2013). Polysacharid A syntetizovan\u00fd B. fragilis p\u00f4sob\u00ed ako protiz\u00e1palov\u00e1 molekula, ktor\u00e1 indukuje sekr\u00e9ciu IL-10 CD4\u00fe T bunkami (Johnson et al., 2015). Bolo zisten\u00e9, \u017ee Clostridia udr\u017eiava hladinu kyseliny retinovej v \u010dreve inhib\u00edciou aktivity retinol dehydrogen\u00e1zy 7 (Rdh7) v \u010drevn\u00fdch epitelov\u00fdch bunk\u00e1ch (Grizotte-Lake et al., 2018). Komens\u00e1ly v \u010dreve tak zohr\u00e1vaj\u00fa v\u00fdznamn\u00fa \u00falohu v modul\u00e1cii zdravia hostite\u013ea r\u00f4znymi sp\u00f4sobmi, ako je metabolizmus \u017eiv\u00edn, vylu\u010dovanie liekov, udr\u017eiavanie integrity bari\u00e9ry a imunomodul\u00e1cia. Bifidobakt\u00e9rie a Lactobacillus spp. sa tie\u017e \u0161iroko pou\u017e\u00edvaj\u00fa ako probiotik\u00e1 v nutraceutickom priemysle a niektor\u00e9 druhy maj\u00fa dlh\u00fa hist\u00f3riu bezpe\u010dn\u00e9ho pou\u017e\u00edvania pri v\u00fdrobe potrav\u00edn, krm\u00edv a s\u00fa \u00fa\u010dinn\u00e9 pri omladzovan\u00ed dysbiotick\u00e9ho \u010dreva v d\u00f4sledku infekcie alebo pou\u017e\u00edvania antibiot\u00edk. Ich pou\u017eitie je v\u0161ak ohrozen\u00e9 translok\u00e1ciou g\u00e9nu rezistencie na erytromyc\u00edn erm(X), ktor\u00fa sprostredkov\u00e1va genomick\u00fd ostrov BKGI1 (Li et al., 2022).<\/p>\n\n\n\n Patog\u00e9nne bakt\u00e9rie v \u010dreve <\/em><\/strong><\/p>\n\n\n\n Ka\u017ed\u00fd rok infekcie tr\u00e1viaceho traktu zab\u00edjaj\u00fa mili\u00f3ny \u013eud\u00ed po celom svete. Ke\u010f\u017ee bakt\u00e9rie s\u00fa naj\u010dastej\u0161ou pr\u00ed\u010dinou ochoren\u00ed tr\u00e1viaceho traktu, na ich lie\u010dbu sa \u010dasto pou\u017e\u00edvaj\u00fa antibiotik\u00e1. Pou\u017e\u00edvanie antibiot\u00edk vedie k dysbi\u00f3ze \u010driev a v extr\u00e9mnych situ\u00e1ci\u00e1ch k sepsii v d\u00f4sledku uvo\u013enenia endotox\u00ednov vyvolan\u00fdch antibiotikami (Lepper et al., 2002). Escherichia, Salmonella, Shigella, Vibrio, Yersinia, patriace do kme\u0148a Proteo bakt\u00e9ri\u00ed, a Clostridia, patriace do kme\u0148a Firmicutes, s\u00fa niektor\u00e9 be\u017en\u00e9 rody \u010drevn\u00fdch patog\u00e9nov. U t\u00fdchto bakteri\u00e1lnych patog\u00e9nov bolo zisten\u00e9, \u017ee obsahuj\u00fa nieko\u013eko g\u00e9nov tox\u00ednov, ktor\u00e9 s\u00fa spojen\u00e9 s MGE, \u010do by mohlo u\u013eah\u010di\u0165 ich prenos na oportunistick\u00e9 patog\u00e9ny a komenz\u00e1lne bakt\u00e9rie v \u010dreve. G\u00e9ny tox\u00ednov \u010drevn\u00fdch patog\u00e9nov a ich spojitos\u0165 s r\u00f4znymi MGE, ktor\u00e9 m\u00f4\u017eu pom\u00e1ha\u0165 pri prenose t\u00fdchto g\u00e9nov tox\u00ednov, s\u00fa podrobne op\u00edsan\u00e9 v nasleduj\u00facich \u010dastiach.<\/p>\n\n\n\n B. fragilis<\/em><\/strong> <\/p>\n\n\n\n B. fragilis je ty\u010dinkovit\u00fd, gramnegat\u00edvny oblig\u00e1tny anaer\u00f3b patriaci do kme\u0148a Bacteroidota. Gen\u00f3m B. fragilis National Collection of Type Cultures (NCTC) 9343 je \u0161iroko \u0161tudovan\u00fd a obsahuje jeden kruhov\u00fd chromoz\u00f3m s d\u013a\u017ekou 5205140 bp, ktor\u00fd obsahuje 4274 g\u00e9nov a plazmid pBF9343 (Pierce a Bernstein, 2016). Hoci t\u00e1to bakt\u00e9ria je u \u013eud\u00ed komenz\u00e1lna, jej podskupina naz\u00fdvan\u00e1 Enterotoxig\u00e9nny B. fragilis (ETBF) bola spojen\u00e1 s v\u00e1\u017enymi ochoreniami \u013eud\u00ed, ako je kolorekt\u00e1lny karcin\u00f3m a z\u00e1palov\u00e1 hna\u010dka. Pri porovnan\u00ed klinick\u00fdch izol\u00e1tov ETBF s referen\u010dn\u00fdm kme\u0148om NCTC 9343 sa zistilo, \u017ee klinick\u00e9 izol\u00e1ty mali 23 % z\u00edskan\u00fdch g\u00e9nov, ktor\u00e9 boli zodpovedn\u00e9 za tox\u00edny a rezistenciu vo\u010di antibiotik\u00e1m (Pierce a Bernstein, 2016). Bolo zisten\u00e9, \u017ee patog\u00e9nny ostrov m\u00e1 zn\u00ed\u017een\u00fd obsah G \u00feC (35 %) v porovnan\u00ed s okolitou DNA (47 \u2013 50 %), \u010do nazna\u010duje, \u017ee izol\u00e1ty ETBF z\u00edskali patog\u00e9nny ostrov prostredn\u00edctvom HGT od in\u00fdch bakt\u00e9ri\u00ed v \u010dreve alebo od in\u00e9ho patog\u00e9nu po\u010das prechodnej infekcie. Okrem toho bolo zisten\u00e9, \u017ee g\u00e9n tox\u00ednu bft-2 a g\u00e9n metaloprote\u00e1zy (mpII) (Moncrief et al., 1995) s\u00fa obklopen\u00e9 predpokladan\u00fdmi mobiliza\u010dn\u00fdmi g\u00e9nmi bfmA, bfmB a bfmC, a samotn\u00fd BfPAI je obklopen\u00fd mobiliza\u010dnou oblas\u0165ou podobnou tej v plazmide pIP417, zn\u00e1mej pre rezistenciu na 5-nitro-imidazol, a plazmide pBFTM10, zn\u00e1mej pre poskytovanie rezistencie na klindamyc\u00edn (Haggoud et al., 1994). Prote\u00edny syntetizovan\u00e9 z g\u00e9nu bfmC boli identifikovan\u00e9 ako podobn\u00e9 mobiliza\u010dn\u00e9mu prote\u00ednu TraD plazmidu F a R100 E. coli (Franco Augusto et al., 1999). Kme\u0148 ETBF tie\u017e obsahuje g\u00e9n tox\u00ednu metaloprote\u00e1zy s molekulovou hmotnos\u0165ou 20 kDa naz\u00fdvan\u00fd fragilysin, ktor\u00fd je zodpovedn\u00fd za cytotoxicitu \u010drevn\u00fdch buniek v patog\u00e9nnom ostrov\u010deku fragilysinu pr\u00edtomnom na transpozit\u00edvnom prvku CTn86. Okrem CTn86 existuj\u00fa aj in\u00e9 predpokladan\u00e9 konjugat\u00edvne transpoz\u00f3ny CTn9343, CTn9343-podobn\u00e9 alebo CTn86-podobn\u00e9 prvky v oblastiach lemuj\u00facich patogenitn\u00e9 ostrov\u010deky ETBF (Buckwold et al., 2007).<\/p>\n\n\n\n C. perfringens<\/em><\/strong> <\/p>\n\n\n\n C. perfringens je sp\u00f3roformuj\u00faci, ty\u010dinkovit\u00fd, grampozit\u00edvny anaer\u00f3bny organizmus patriaci do kme\u0148a Bacillota\/Firmicutes, ktor\u00fd sa be\u017ene vyskytuje v \u010dreve zdrav\u00fdch \u013eud\u00ed. Niekedy v\u0161ak C. perfringens sp\u00f4sobuje r\u00f4zne \u010drevn\u00e9 \u0165a\u017ekosti a \u010drevn\u00e9 ochorenia, ako je otravu jedlom, hna\u010dku nez\u00e1visl\u00fa od jedla a kolit\u00eddu (Uzal et al., 2010). Kompletn\u00e1 sekvencia gen\u00f3mu 56 enterotox\u00edn produkuj\u00facich C. perfringens izolovan\u00fdch od pacientov s otravou jedlom preuk\u00e1zala, \u017ee maj\u00fa r\u00f4znorod\u00fd pangen\u00f3m s iba 12,6 % koregen\u00f3mom, \u010do nazna\u010duje v\u00fdskyt vysokej miery HGT a z\u00edskanie nov\u00fdch g\u00e9nov, ktor\u00e9 prispievaj\u00fa k produkcii tox\u00ednov, rezistencii vo\u010di antibiotik\u00e1m a perzistencii (Kiu a Hall, 2018). Kme\u0148om C. perfringens typu A bol identifikovan\u00fd predpokladan\u00fd otvoren\u00fd \u010d\u00edtac\u00ed r\u00e1mec (ORF), ktor\u00fd vykazuje homol\u00f3giu s ORF Salmonella Typhimurium IS200 inzer\u010dn\u00fdm prvkom 1,5 kb nad g\u00e9nom cpe, ktor\u00fd k\u00f3duje enterotox\u00edn C. perfringens zodpovedn\u00fd za toxik\u00f3zu (Brynestad et al., 1997). \u010ealej bolo zisten\u00e9, \u017ee g\u00e9n epsilon tox\u00ednu (etx) pr\u00edtomn\u00fd v kme\u0148och typu B a D C. perfringens je obklopen\u00fd IS1151 a g\u00e9nom spojen\u00fdm s transpoz\u00f3nom Tn3, ktor\u00fd vykazuje podobnos\u0165 s g\u00e9nom k\u00f3duj\u00facim transpoz\u00e1zu v S. aureus a Lactococcus (Brynestad et al., 1997; Uzal et al., 2010). IS1151 umiestnen\u00fd 96 bp nad g\u00e9nom etx v kme\u0148och C. perfringens typu D bol identifikovan\u00fd ako homologick\u00fd s prvkami inzer\u010dnej sekvencie (IS) Bacillus thuringiensis a E. coli (Daube et al., 1993). Nieko\u013eko kme\u0148ov C. perfringens typu A bolo tie\u017e identifikovan\u00fdch ako nosite\u013eov g\u00e9nu cpe na ve\u013ekej plazmide, ktor\u00e1 obsahovala prvok IS1470 vo svojom chromoz\u00f3me (Brynestad et al., 1994). Prvok IS1470 niesol g\u00e9n k\u00f3duj\u00faci enz\u00fdm transpoz\u00e1zu 346 aa, ktor\u00fd vykazoval homol\u00f3giu s transpoz\u00e1zou nes\u00facou IS30 (Brynestad et al., 1994). Okrem toho bolo zisten\u00e9, \u017ee gen\u00f3m C. perfringens je bohat\u00fd na f\u00e1gov\u00e9 prvky, ako s\u00fa \u03d5SM101, \u03d53626, \u03d5S9, \u03d5S63, \u03d5CP26F, \u03d5CP390, \u03d5CPV4, \u03d5ZP2, \u03d5CP7R, \u03d5CPV1 a \u03d5CP24R (Kim et al., 2012).<\/p>\n\n\n\n C. botulinum<\/em><\/strong> <\/p>\n\n\n\n C. botulinum je ty\u010dinkovit\u00fd, pohybliv\u00fd, sp\u00f3roformuj\u00faci, grampozit\u00edvny anaer\u00f3bny organizmus patriaci do kme\u0148a Bacillota\/Firmicutes, ktor\u00fd produkuje neurotox\u00edn botul\u00edn. Botulizmus u \u013eud\u00ed je sp\u00f4soben\u00fd konzum\u00e1ciou kontaminovan\u00fdch potrav\u00edn a m\u00f4\u017ee sp\u00f4sobi\u0165 neurotoxicitu a dokonca paral\u00fdzu (Nigam a Nigam, 2010). Existuj\u00fa \u0161tyri skupiny C. botulinum, z ktor\u00fdch skupiny I a II sp\u00f4sobuj\u00fa botulizmus u \u013eud\u00ed. Skupina III sp\u00f4sobuje botulizmus u zvierat a skupina IV nem\u00e1 \u017eiadnu s\u00favislos\u0165 s botulizmom (Peck, 2009). Pod\u013ea spr\u00e1vy z roku 2017 bol v NCBI (http:\/\/www.ncbi.nlm.nih.gov\/genbank\/) k dispoz\u00edcii kompletn\u00fd gen\u00f3m iba 13 kme\u0148ov C. botulinum. V roku 2022 v\u0161ak existuje pribli\u017ene 35 kompletn\u00fdch gen\u00f3mov\u00fdch sekvenci\u00ed a 440 \u010diasto\u010dn\u00fdch gen\u00f3mov\u00fdch sekvenci\u00ed C. botulinum. Ve\u013ekos\u0165 gen\u00f3mu C. botulinum sa pohybovala od 3,2 do 4,2 Mb s obsahom GC 27\u201329 % (Bhardwaj a Somvanshi, 2017). G\u00e9nov\u00fd klaster bont k\u00f3duje botulotox\u00edn (BoNT), ktor\u00fd inaktivuje acetylchol\u00ednov\u00e9 kotvy v neuromuskul\u00e1rnych spojeniach a sp\u00f4sobuje paral\u00fdzu. Pr\u00edtomnos\u0165 g\u00e9nov bont v C. botulinum je identifikovan\u00e1 v\u010faka HGT. G\u00e9nov\u00fd klaster bont je pr\u00edtomn\u00fd bu\u010f v chromoz\u00f3me, alebo v plazmide bakt\u00e9rie. V kmene C. botulinum A ATCC 3502 s\u00fa g\u00e9ny bont pr\u00edtomn\u00e9 v oper\u00f3ne oppA\/brnQ, oper\u00f3ne arsC alebo oper\u00f3ne rarA (Skarin a Segerman, 2011). BoNT sa \u010falej del\u00ed na typy A, B, C, D, E, F a G. Skupina II C. botulinum je vo ve\u013ekej miere izolovan\u00e1 z infekci\u00ed pren\u00e1\u0161an\u00fdch potravinami a je zn\u00e1ma produkciou neurotox\u00ednov B, E a F. V C. botulinum s\u00fa tox\u00edny A, B a F k\u00f3dovan\u00e9 chromoz\u00f3mom, tox\u00edn G je k\u00f3dovan\u00fd plazmidom a prof\u00e1gy k\u00f3duj\u00fa C1, D a E (Br\u00fcssow et al., 2004; Skarin a Segerman, 2011). Bolo zisten\u00e9, \u017ee tox\u00edn C. botulinum G je pr\u00edtomn\u00fd na plazmide 81MD, a bolo zisten\u00e9, \u017ee kme\u0148 C. botulinum typu C (C)-203 U28 obsahuje tox\u00edn C2 na ve\u013ekom plazmide ozna\u010denom ako pC2C203U28. \u010eal\u0161ia podrobn\u00e1 gen\u00f3mov\u00e1 anal\u00fdza C. botulinum odhalila, \u017ee kmene skupiny III obsahuj\u00fa r\u00f4zne in\u00e9 tox\u00edny k\u00f3dovan\u00e9 v plazmidoch (Nawrocki et al., 2018). Ned\u00e1vna spr\u00e1va nazna\u010duje, \u017ee C. botulinum skupiny I a II m\u00e1 mnoho bont klastrov obklopen\u00fdch IS prvkami, \u010do umo\u017e\u0148uje mobilitu t\u00fdchto g\u00e9nov v gen\u00f3me a tie\u017e ich prenos do in\u00fdch bakt\u00e9ri\u00ed (Sakaguchi et al., 2009). Okrem toho bolo zisten\u00e9, \u017ee g\u00e9ny C2toxingenes s\u00fa spojen\u00e9 s IS prvkami, ako s\u00fa ISCbt5 a ISCbt6 (Sakaguchi et al., 2009). Hoci bolo v gen\u00f3me C. botulinum identifikovan\u00e9 ve\u013ek\u00e9 mno\u017estvo IS prvkov a plazm\u00edd, okrem t\u00fdch, ktor\u00e9 obsahuj\u00fa g\u00e9ny botC a D, nie je k dispoz\u00edcii ve\u013ea inform\u00e1ci\u00ed o prevalencii f\u00e1gov\u00fdch prvkov v gen\u00f3me (Hilletal., 2009). Bolo v\u0161ak zisten\u00e9, \u017ee p\u00e4\u0165 f\u00e1gov sc-st, c-468, c-203, c-d6f a d-1873 je zodpovedn\u00fdch za premenu netoxigenick\u00fdch kme\u0148ov C. botulinum typu C a D na toxigenick\u00e9 kmene (Sakaguchi et al., 2005). Okrem toho sa zistilo, \u017ee infekcia dvoma bakteriof\u00e1gmi, CE\u03b2 a Ce\u03b3, men\u00ed netoxick\u00e9 kmene na toxick\u00e9 (Eklund et al., 1971).<\/p>\n\n\n\n C. difficile<\/em><\/strong> <\/p>\n\n\n\n C. difficile je anaer\u00f3bna, grampozit\u00edvna, ty\u010dinkovit\u00e1 bakt\u00e9ria patriaca do kme\u0148a Bacillota, Firmicutes, ktor\u00e1 je zn\u00e1ma t\u00fdm, \u017ee u \u013eud\u00ed sp\u00f4sobuje hna\u010dkov\u00e9 ochorenia a kolit\u00eddu. V roku 2022 bolo v Genbank ulo\u017een\u00fdch viac ako 2600 gen\u00f3mov C. difficile. Odhaduje sa, \u017ee kompletn\u00fd pangen\u00f3m C. difficile obsahuje pribli\u017ene 9640 g\u00e9nov, ktor\u00e9 boli z\u00edskan\u00e9 hlavne prostredn\u00edctvom HGT udalost\u00ed, ktor\u00e9 tvoria pribli\u017ene 11 percent celkov\u00e9ho gen\u00f3mu (Eyre et al., 2013; Scaria et al., 2010). Bolo identifikovan\u00fdch mnoho plazm\u00eddov, ktor\u00e9 obsahuj\u00fa g\u00e9ny, ktor\u00e9 dod\u00e1vaj\u00fa C. difficile rezistenciu vo\u010di antibiotik\u00e1m. Mnoho \u0161t\u00fadi\u00ed v minulosti hl\u00e1silo pr\u00edtomnos\u0165 transpoz\u00f3nov, ktor\u00e9 dod\u00e1vaj\u00fa rezistenciu vo\u010di antibiotik\u00e1m, ako s\u00fa Tn5397 alebo CTn3 (rezistencia vo\u010di tetracykl\u00ednu), Tn5398 (rezistencia vo\u010di makrolidom, linkozamidom a streptogram\u00ednom). Faktory virulence C. difficile s\u00fa tox\u00edny A (klostridi\u00e1lny cytotox\u00edn) a B, k\u00f3dovan\u00e9 g\u00e9nmi tcdA a tcdB na 19,6 kb dlhom \u00faseku chromoz\u00f3mu, ktor\u00fd tvor\u00ed odli\u0161n\u00fd patog\u00e9nny lokus (PaLoc). \u010ealej bolo zisten\u00e9, \u017ee g\u00e9ny tcdB a cdtAB, ktor\u00e9 k\u00f3duj\u00fa bin\u00e1rny tox\u00edn s ADP ribosyltransfer\u00e1zovou aktivitou, s\u00fa k\u00f3dovan\u00e9 pravdepodobn\u00fdmi konjuga\u010dn\u00fdmi plazmidmi. Bolo zisten\u00e9, \u017ee kmene C. difficile Clade C-I nes\u00fa monotox\u00edn tcdB\u00fePaLoc ved\u013ea plnej CdtLoc ved\u013ea extrachromos\u00f3mov\u00fdch molek\u00fal, ktor\u00e9 sa podobaj\u00fa konjuga\u010dn\u00fdm plazmidom (Ram\u00edrez-Vargas a Rodr\u00edguez, 2020). Okrem toho PaLoc k\u00f3duje prote\u00edny, ktor\u00e9 reguluj\u00fa a pom\u00e1haj\u00fa pri sekr\u00e9cii tox\u00ednu. Bolo zisten\u00e9, \u017ee prenos PaLoc konvertuje netoxig\u00e9nny kme\u0148 na toxig\u00e9nny (Brouwer et al., 2013). PaLoc ch\u00fdba v netoxick\u00fdch kme\u0148och. Medzi dvoma ISscdu2\/20 a cdd2\u20133 nach\u00e1dzaj\u00facimi sa nad a pod PaLoc bol n\u00e1jden\u00fd fragment DNA s d\u013a\u017ekou 115 bp (Braun et al., 1996). K\u00fdm v in\u00fdch kme\u0148och, ako je VPI 10463, m\u00e1 toxig\u00e9nny prvok d\u013a\u017eku 19,6 kb a obsahuje p\u00e4\u0165 ORF. \u0160tyri z t\u00fdchto ORF s\u00fa tox\u00edn A, tox\u00edn B, ORFtxe2 a ORFtxe3 a ORFtxel (Hammond a Johnson, 1995). Zauj\u00edmav\u00e9 je, \u017ee presn\u00fd mechanizmus prenosu PaLoc medzi kme\u0148mi nie je \u00faplne zn\u00e1my. K dne\u0161n\u00e9mu d\u0148u nie je k dispoz\u00edcii ve\u013ea \u00fadajov o pr\u00edtomnosti transpoz\u00f3nov, ktor\u00e9 s\u00fa spojen\u00e9 s mobilitou g\u00e9nov virulencie alebo tox\u00ednov v C. difficile (Brouwer et al., 2011). IStrony s\u00fa kombin\u00e1ciou intr\u00f3nu skupiny I a ANIS, ktor\u00e9 sa m\u00f4\u017eu \u00faplne vyreza\u0165 a transponova\u0165 na nov\u00e9 miesto. IStrony s\u00fa schopn\u00e9 obsahova\u0165 variantn\u00e9 prote\u00edny, preto\u017ee maj\u00fa jedine\u010dn\u00fa spojovaciu aktivitu. Zistilo sa, \u017ee vlo\u017eenie IStronu do tox\u00ednu A C. difficile je zodpovedn\u00e9 za produkciu alternat\u00edvnych variantn\u00fdch tox\u00ednov bakt\u00e9riou. Rupnik et al. (2016) \u0161tudovali r\u00f4zne permut\u00e1cie tox\u00ednov produkovan\u00fdch r\u00f4znymi typmi tox\u00ednov C. difficile.<\/p>\n\n\n\n E. faecalis<\/em><\/strong> <\/p>\n\n\n\n E. faecalis je grampozit\u00edvny organizmus, ktor\u00fd patr\u00ed do kme\u0148a Bacillota, Firmicutes a je prirodzen\u00fdm obyvate\u013eom gastrointestin\u00e1lneho traktu \u013eud\u00ed a zriedkavo sa vyskytuje v stolici. Hoci sa t\u00e1to bakt\u00e9ria pova\u017euje za komenz\u00e1lnu, bola tie\u017e sp\u00e1jan\u00e1 s mnoh\u00fdmi nozokomi\u00e1lnymi (s zdravotn\u00edckou starostlivos\u0165ou s\u00favisiacimi) infekciami, vr\u00e1tane infekci\u00ed mo\u010dov\u00fdch ciest, bakter\u00e9mie, infekci\u00ed r\u00e1n a endokardit\u00eddy (Fowler et al., 2005; Murray, 1990; Tleyjeh et al., 2005). Referen\u010dn\u00fd kme\u0148 E. faecalis V583, klinick\u00fd izol\u00e1t, bol po prv\u00fdkr\u00e1t zaznamenan\u00fd, sekvenovan\u00fd a publikovan\u00fd v roku 2003 v USA. Obsahoval 3337 ORF, ktor\u00e9 k\u00f3duj\u00fa prote\u00edny v jeho chromoz\u00f3me a troch plazmidoch pTEF1, pTEF2 a pTEF3. Obsah G \u00fe C v chromoz\u00f3me kme\u0148a bol 37,5 %, zatia\u013e \u010do plazmidy vykazovali obsah G \u00fe C 33,3 \u2013 34,4 % a k\u00f3dovali 3240 prote\u00ednov. Celkovo 25 % gen\u00f3mu E. faecalis pozost\u00e1va hlavne z nieko\u013ek\u00fdch MGE, ako je 38 inzer\u010dn\u00fdch elementov, 7 f\u00e1gov\u00fdch regi\u00f3nov, patog\u00e9nnych ostrovov a regi\u00f3nov pre kompozitn\u00e9 transpozibiln\u00e9 elementy. V\u00e4\u010d\u0161ina MGE bola identifikovan\u00e1 ako nosite\u013eka ARG a virulentn\u00fdch g\u00e9nov (Giridhara Upadhyaya et al., 2009; Paulsen et al., 2003). . V E. faecalis faktory virulence zah\u0155\u0148aj\u00fa hlavne adh\u00e9ziu, tvorbu biofilmu, quorum sensing a tox\u00ednov\u00e9 g\u00e9ny. Adh\u00e9zne faktory, ako s\u00fa ebpA\/ B\/C (pili pom\u00e1haj\u00face pri adh\u00e9zii bakt\u00e9ri\u00ed k prote\u00ednom hostite\u013ea), ace (kolag\u00e9nov\u00fd adhez\u00edn) a asa1 (agrega\u010dn\u00e1 l\u00e1tka), boli spojen\u00e9 s virulenciou organizmu (Fiore et al., 2019) . Bolo zisten\u00e9, \u017ee tox\u00edn cytolyz\u00edn E. faecalis je produkovan\u00fd g\u00e9nmi pr\u00edtomn\u00fdmi v cyl oper\u00f3ne (tox\u00edn cytolyz\u00edn), ktor\u00fd pozost\u00e1va z 8 g\u00e9nov cylA\/B\/I\/M\/R1\/R2\/S (Fiore et al., 2019). Okrem toho bolo zisten\u00e9, \u017ee nieko\u013eko kme\u0148ov E. faecalis produkuje bakterioc\u00edny, ktor\u00e9 s\u00fa k\u00f3dovan\u00e9 konjuga\u010dnou plazmidou pMB1 s ve\u013ekos\u0165ou 90 kb a reaguj\u00fa na pohlavn\u00e9 ferom\u00f3ny uvo\u013e\u0148ovan\u00e9 in\u00fdmi bakt\u00e9riami, ktor\u00e9 u\u013eah\u010duj\u00fa ich prenos (Mart\u00ednez-Bueno et al., 1992). Predch\u00e1dzaj\u00face \u0161t\u00fadie odhalili, \u017ee najvirulentnej\u0161ie kmene E. faecalis s\u00fa MDR a silne tvoria biofilm, preto\u017ee maj\u00fa v\u00fdhodu v pre\u017eit\u00ed v \u010dreve v porovnan\u00ed s in\u00fdmi citliv\u00fdmi \u010drevn\u00fdmi bakt\u00e9riami (Mundy et al., 2000). Enterokokov\u00fd povrchov\u00fd prote\u00edn (Esp) k\u00f3dovan\u00fd g\u00e9nom esp je zodpovedn\u00fd za tvorbu biofilmu, ktor\u00fd umo\u017e\u0148uje jeho koloniz\u00e1ciu v gastrointestin\u00e1lnom trakte (Kristich Christopher et al., 2004). Klinick\u00e9 kmene E. faecalis obsahovali patog\u00e9nne ostrovy, ktor\u00e9 obsahovali cytolyz\u00edn aj esp v porovnan\u00ed s neinfek\u010dn\u00fdmi izol\u00e1tmi poch\u00e1dzaj\u00facimi z \u00fastnej dutiny (Gold et al., 1975). Izol\u00e1ty boli tie\u017e identifikovan\u00e9 ako obsahuj\u00face prof\u00e1gov\u00e9 prvky, ktor\u00e9 s\u00fa v\u00e4\u010d\u0161inou spojen\u00e9 s virulenciou a patogenitou. Kme\u0148 V583 obsahuje sedem prof\u00e1gov\u00fdch prvkov, ktor\u00e9 patria do kateg\u00f3rie temperovan\u00fdch f\u00e1gov V583-pp1 a\u017e V583-pp7 s ve\u013ekos\u0165ou od 12 do 43 Kb (Matos et al., 2013). Okrem miernych f\u00e1gov boli hl\u00e1sen\u00e9 aj lyzog\u00e9nne f\u00e1gy, a to GQ478081 (\u03a6FL1A), GQ478082 (\u03a6FL1B), GQ478083 (\u03a6FL1C), GQ478084 (\u03a6FL2A), GQ478085 (\u03a6FL2B), GQ478086 (\u03a6FL3A), GQ478087 (\u03a6FL3B) a GQ478088 (\u03a6FL4A) (Stevens et al., 2011). DNA f\u00e1gu sa integruje do hostite\u013eskej bakt\u00e9rie prostredn\u00edctvom integr\u00e1zy patriacej do rodiny ser\u00ednov\u00fdch rekombin\u00e1z na miestach att v chromoz\u00f3me. Prote\u00edny k\u00f3dovan\u00e9 g\u00e9nom f\u00e1gov sa podie\u013eaj\u00fa na udr\u017ean\u00ed lysog\u00e9nie, adh\u00e9zii a virulencii (Brede et al., 2011).<\/p>\n\n\n\n S. aureus<\/em><\/strong> <\/p>\n\n\n\n S. aureus je grampozit\u00edvna bakt\u00e9ria, ktor\u00e1 patr\u00ed do kme\u0148a Bacillota, Firmicutes a je oportunistick\u00fdm patog\u00e9nom, ktor\u00fd kolonizuje r\u00f4zne \u010dasti \u013eudsk\u00e9ho tela. Je v\u0161ak tie\u017e zn\u00e1me, \u017ee t\u00e1to bakt\u00e9ria sp\u00f4sobuje ochorenia, ako je otrava jedlom, toxick\u00fd \u0161okov\u00fd syndr\u00f3m, pneum\u00f3nia, sepsa a endokardit\u00edda. S. aureus je hlavnou pr\u00ed\u010dinou nozokomi\u00e1lnych infekci\u00ed a je notoricky zn\u00e1my t\u00fdm, \u017ee z\u00edskava virulentn\u00e9 g\u00e9ny k\u00f3dovan\u00e9 MGE (Lindsay a Holden, 2004). Gen\u00f3m S. aureus sa pohybuje od 2,8 Mb do 2,9 Mb. Pribli\u017ene 75 % gen\u00f3mu S. aureus bolo identifikovan\u00fdch ako konzervovan\u00fdch, ktor\u00e9 tvoria jadrov\u00fd gen\u00f3m a podie\u013eaj\u00fa sa na pravidelnom metabolizme bunky. Pribli\u017ene 25 % gen\u00f3mu bolo identifikovan\u00fdch ako doplnkov\u00fd gen\u00f3m, ktor\u00fd obsahoval ni\u017e\u0161\u00ed obsah G \u00fe C v porovnan\u00ed s jadrov\u00fdm gen\u00f3mom (Turner et al., 2019). Podobne ako u in\u00fdch bakt\u00e9ri\u00ed, doplnkov\u00fd gen\u00f3m tvoria g\u00e9ny spojen\u00e9 s virulenciou a patogenitou. Izol\u00e1ty S. aureus prirodzene obsahuj\u00fa jeden alebo viac plazm\u00eddov a s\u00fa klasifikovan\u00e9 do troch tried, I, II a III. Bolo zisten\u00e9, \u017ee v S. aureus sa v\u00e4\u010d\u0161ina prenosu plazmidov uskuto\u010d\u0148uje prostredn\u00edctvom transdukcie, preto\u017ee S. aureus nie je konjugat\u00edvne kompetentn\u00fd. Mnoh\u00e9 ARG S. aureus s\u00fa spojen\u00e9 s plazmidmi. vanAoperon, ktor\u00fd obsahuje g\u00e9ny, ktor\u00e9 poskytuj\u00fa rezistenciu vo\u010di vankomyc\u00ednu, je pod\u013ea v\u0161etk\u00e9ho z\u00edskan\u00fd E. faecalis v d\u00f4sledku konjugat\u00edvneho prenosu (Hiramatsu et al., 1997). Okrem g\u00e9nov, ktor\u00e9 k\u00f3duj\u00fa rezistenciu vo\u010di vankomyc\u00ednu, boli v plazmidoch S. aureus identifikovan\u00e9 aj g\u00e9ny, ktor\u00e9 k\u00f3duj\u00fa rezistenciu vo\u010di beta-lakt\u00e1mov\u00fdm antibiotik\u00e1m (Altboum et al., 1985). Okrem toho boli identifikovan\u00e9 enterotox\u00edn B, bakterioc\u00edn a exfoliat\u00edvny tox\u00edn B ako plazmidy k\u00f3dovan\u00e9 v patog\u00e9ne (Bukowski et al., 2010). \u0160es\u0165 g\u00e9nov (seg, sei, sem, sen, seo a seu) k\u00f3duj\u00facich enterotox\u00edny sa nach\u00e1dza v klastri g\u00e9nov enterotox\u00ednu (egc), ktor\u00fd je s\u00fa\u010das\u0165ou gen\u00f3mov\u00e9ho ostrova S. aureus vSa\u03b2 (tie\u017e zn\u00e1my ako SaPI3\/m3). Prenos vSa\u03b2 u\u013eah\u010duje stafylokokov\u00fd mierny f\u00e1g \u03a6 SaBov (Moon et al., 2015). Okrem plazm\u00eddov boli v gen\u00f3me S. aureus identifikovan\u00e9 aj genetick\u00e9 prvky, ako s\u00fa transpoz\u00f3ny a IS prvky, ktor\u00e9 pom\u00e1haj\u00fa pri bakteri\u00e1lnej evol\u00facii, a to v jedinom alebo tandemovom k\u00f3pi\u00e1ch. Je tie\u017e zn\u00e1me, \u017ee IS a jednotkov\u00e9 transpoz\u00f3ny v\u00fdrazne prispievaj\u00fa k antibiotick\u00e9mu odporu u S aureus (Byrne et al., 1989). Okrem antibiotick\u00e9ho odporu transpoz\u00f3ny tie\u017e poskytuj\u00fa odolnos\u0165 vo\u010di \u0165a\u017ek\u00fdm kovom, ako je kadmium (Kuroda et al., 2001). F\u00e1gov\u00e9 prvky S. aureus s\u00fa troch typov: lytick\u00e9, temperovan\u00e9 a chronick\u00e9. Na z\u00e1klade ve\u013ekosti f\u00e1gov\u00e9ho prvku sa \u010falej delia na triedu I (16\u201320 kb), II (35\u201340 kb) a III (125\u2013140 kb) (Kwan et al., 2005). V S. aureus obsahuj\u00fa temperovan\u00e9 bakteriof\u00e1gy g\u00e9ny ako stafylokin\u00e1za (sak), prote\u00edn inhibuj\u00faci chemotaxiu (scn), enterotox\u00edny a exfoliat\u00edvny tox\u00edn (eta) (Deghorain a Van Melderen, 2012). Virulentn\u00e9 faktory, ako je Panton-Valentine leukocid\u00edn, enterotox\u00edn A a exfoliat\u00edvny tox\u00edn A, s\u00fa k\u00f3dovan\u00e9 lysog\u00e9nnymi prof\u00e1gmi. G\u00e9ny asociovan\u00e9 s virulenciou sa zvy\u010dajne nach\u00e1dzaj\u00fa v bl\u00edzkosti miesta pripojenia (att) a integra\u010dn\u00e9ho miesta (int) f\u00e1gov\u00e9ho elementu. Pomocn\u00e9 f\u00e1gy \u03a611 a \u03a680\u03b1 pom\u00e1haj\u00fa pri replik\u00e1cii, mobiliz\u00e1cii a exc\u00edzii ostrovov patogenity stafylokokov (SaPI), ktor\u00e9 s\u00fa nemobiln\u00fdmi patog\u00e9nnymi ostrovmi S. aureus (Mir-Sanchis et al., 2012; Ram et al., 2012). Bolo sekvencovan\u00fdch mnoho SaPI, ktor\u00e9 k\u00f3duj\u00fa enterotox\u00edny a tox\u00edn toxick\u00e9ho \u0161okov\u00e9ho syndr\u00f3mu (TSST) (Xia a Wolz, 2014).<\/p>\n\n\n\n Salmonella spp <\/p>\n\n\n\n Salmonella je gramnegat\u00edvna enterobakt\u00e9ria v tvare ty\u010dinky, ktor\u00e1 patr\u00ed do kme\u0148a Pseudomonadota, teda Proteobacteria. Ide o fakultat\u00edvne anaer\u00f3bne bakt\u00e9rie, ktor\u00e9 s\u00fa zodpovedn\u00e9 za zna\u010dn\u00fa \u010das\u0165 ochoren\u00ed na celom svete. Salmonella spp. je zn\u00e1ma ako jedna z hlavn\u00fdch pr\u00ed\u010din gastrointestin\u00e1lnych ochoren\u00ed po celom svete. Celosvetovo je 1,3 miliardy pr\u00edpadov gastroenterit\u00eddy, 3 mili\u00f3ny \u00famrt\u00ed a 16 mili\u00f3nov pr\u00edpadov bru\u0161n\u00e9ho t\u00fdfusu pripisovan\u00fdch ka\u017edoro\u010dne Salmonelle (Pui et al., 2011). Salmonella enterica a Salmonella bongori s\u00fa dva druhy, ktor\u00e9 tvoria rod Salmonella. Viac ako 2600 s\u00e9rotypov S. enterica je \u010falej rozdelen\u00fdch do \u0161iestich poddruhov, ktor\u00e9 sa od seba odli\u0161uj\u00fa rozdielmi v ich bi\u010d\u00edkov\u00fdch (H) a somatick\u00fdch (O) vlastnostiach. V\u00e4\u010d\u0161ina infekci\u00ed u \u013eud\u00ed je sp\u00f4soben\u00e1 S. enterica poddruhom I (enterica), ktor\u00fd je z\u00e1rove\u0148 naj\u010dastej\u0161ie izolovan\u00fdm poddruhom u zvierat (Brenner et al., 2000). Na druhej strane, S. bongori sa Vibrio parahaemolyticus<\/em><\/strong> <\/p>\n\n\n\n Vibrio parahaemolyticus je gramnegat\u00edvna, zakriven\u00e1, ty\u010dinkovit\u00e1, halofiln\u00e1 bakt\u00e9ria patriaca do kme\u0148a Pseudomonadota, Proteobacteria, ktor\u00e1 sp\u00f4sobuje gastrointestin\u00e1lne ochorenia u \u013eud\u00ed po konzum\u00e1cii nespr\u00e1vne pripraven\u00fdch morsk\u00fdch \u017eivo\u010d\u00edchov (Danielsetal., 2000). V. parahaemolyticus bol prv\u00fdkr\u00e1t objaven\u00fd v roku 1950 po vypuknut\u00ed otravy morsk\u00fdmi plodmi v Japonsku (Medzin\u00e1rodn\u00e9 symp\u00f3zium o Vibrio parahaemolyticus, 1974). Okrem toho bola V. parahaemolyticus sp\u00e1jan\u00e1 s pr\u00ed\u010dinou septik\u00e9mie a infekci\u00ed r\u00e1n u \u013eud\u00ed (Santos et al., 2020). Okrem infekci\u00ed u \u013eud\u00ed sp\u00f4sobuje tento patog\u00e9n aj infekcie u kreviet [ak\u00fatna hepatopankreatick\u00e1 nekr\u00f3za (AHPND)], \u010do je novo sa objavuj\u00face ochorenie, p\u00f4vodne naz\u00fdvan\u00e9 syndr\u00f3m v\u010dasnej \u00famrtnosti (Tena et al., 2010). AHPND nie je sp\u00f4soben\u00e9 len V. parahaemolyticus, ale aj in\u00fdmi \u010dlenmi rodu Vibrio sp., ako s\u00fa V. campbellii, V. owensii a V. punensis. Zauj\u00edmav\u00e9 je, \u017ee bolo zisten\u00e9, \u017ee plazmid typu pVA1 nesie g\u00e9n tox\u00ednu pirABvp zodpovedn\u00fd za t\u00fato chorobu. \u010ealej bolo zisten\u00e9, \u017ee plazmid sa m\u00f4\u017ee pren\u00e1\u0161a\u0165 medzi druhmi rodu Vibrio prostredn\u00edctvom konjug\u00e1cie. Bolo zisten\u00e9, \u017ee plazmid typu pVA1 m\u00e1 obsah GC pribli\u017ene 45,9 % s po\u010dtom k\u00f3pi\u00ed 37 na bakteri\u00e1lnu bunku a pozost\u00e1va z 92 ORF, ktor\u00e9 k\u00f3duj\u00fa prote\u00edny asociovan\u00e9 s virulenciou, mobiliza\u010dn\u00e9 prote\u00edny, replika\u010dn\u00e9 enz\u00fdmy, transpoz\u00e1zy a in\u00e9 prote\u00edny, ktor\u00e9 s\u00favisia s tox\u00ednmi z Photorhabdus insect-related (Pir) tox\u00ednov (Lee et al., 2015). Dva g\u00e9ny, pirA- a pirB-like, ktor\u00e9 sa nach\u00e1dzaj\u00fa v oblasti fragmentu s ve\u013ekos\u0165ou 3,5 kb, s\u00fa obklopen\u00e9 1 kb invertovan\u00fdmi opakovan\u00fdmi sekvenciami k\u00f3duj\u00facimi transpoz\u00f3ny a s\u00fa spojen\u00e9 s k\u00f3dovan\u00edm prote\u00ednov podobn\u00fdch tox\u00ednu Pir v V. parahaemolyticus. Obsah GC t\u00fdchto dvoch g\u00e9nov bol podstatne ni\u017e\u0161\u00ed (38,2 %) ako v ostatnej \u010dasti plazmidu, \u010do nazna\u010duje, \u017ee tieto g\u00e9ny boli z\u00edskan\u00e9 horizont\u00e1lnym prenosom. V. parahaemolyticus a V. cholerae, p\u00f4vodca cholery, maj\u00fa spolo\u010dn\u00fd fylogenetick\u00fd vz\u0165ah. Oba maj\u00fa dva kruhov\u00e9 chromoz\u00f3my. Genom V. parahaemolyticus m\u00e1 dva chromoz\u00f3my, ktor\u00e9 maj\u00fa ve\u013ekos\u0165 pribli\u017ene 3288558 bp a 1877212 bp a obsahuj\u00fa 4832 g\u00e9nov, s obsahom G\u00feC 454 percent pre ka\u017ed\u00fd chromoz\u00f3m. Chromoz\u00f3m I V. parahaemolyticus a V cholerae sa identifikoval ako ve\u013ekos\u0165ou ve\u013emi podobn\u00fd (33 vs. 30 Mb), ale chromoz\u00f3m II V. parahaemolyticus sa identifikoval ako v\u00e4\u010d\u0161\u00ed ne\u017e chromoz\u00f3m V. cholerae (19 vs. 11 Mb) (Tagomori et al., 2002). V V. parahaemolyticus bolo identifikovan\u00fdch nieko\u013eko plazm\u00edd, ako napr\u00edklad pSA19, pZY5 a p22702B. V\u00e4\u010d\u0161ina g\u00e9nov v t\u00fdchto plazmidoch bola zn\u00e1ma ako k\u00f3duj\u00faca hypotetick\u00e9 prote\u00edny. \u0160t\u00fadie o ICE V. parahaemolyticus s\u00fa ojedinel\u00e9, av\u0161ak v roku 2019 \u0161t\u00fadia He et al. (2019) identifikovala ICE pozit\u00edvny V. parahaemolyticus izolovan\u00fd z kreviet chovan\u00fdch v akvakult\u00fare. ICE \u00fadajne obsahuje hlavne g\u00e9ny, ktor\u00e9 k\u00f3duj\u00fa rezistenciu vo\u010di antibiotik\u00e1m a \u0165a\u017ek\u00fdm kovom. Na rozdiel od obmedzen\u00fdch \u0161t\u00fadi\u00ed o plazmidoch a ICE V. parahaemolyticus existuje mno\u017estvo \u0161t\u00fadi\u00ed o f\u00e1gov\u00fdch prvkoch, ktor\u00e9 z\u00edskal tento patog\u00e9n, a o ich pr\u00edspevku k jeho patogenite. Existuj\u00fa spr\u00e1vy o vl\u00e1knit\u00fdch vibriof\u00e1goch, ako je f237 identifikovan\u00fd z pandemick\u00fdch klonov O3:K6 V. parahaemolyticus. Medzi \u010fal\u0161ie dobre charakterizovan\u00e9 f\u00e1gov\u00e9 elementy vo V. parahaemolyticus patria KVP40, VP882, VP93, pO3K6, Vf12, Vf33, VfO3K6, VfO4K68 a VpV262. Bola identifikovan\u00e1 v\u00fdznamn\u00e1 podobnos\u0165 aminokysel\u00edn medzi vl\u00e1knit\u00fdmi f\u00e1gmi V. parahaemolyticus a f\u00e1gmi identifikovan\u00fdmi z in\u00fdch druhov \u010de\u013eade Vibrionaceae (Chang et al, 1998). Okrem toho existuj\u00fa d\u00f4kazy o \u010fal\u0161\u00edch udalostiach HGT v gen\u00f3me V. parahaemolyticus. Bola pozorovan\u00e1 vysok\u00e1 podobnos\u0165 v T3SS lokalizovanom na chromoz\u00f3me II V. parahaemolyticus a kme\u0148och V. cholerae non-O1\/non-O139. Druh\u00fd T3SS2 V. parahaemolyticus lokalizovan\u00fd na chromoz\u00f3me II bol identifikovan\u00fd ako obsahuj\u00faci dve k\u00f3pie tdh (termostabiln\u00fd priamy hemolyz\u00edn) obklopen\u00e9 g\u00e9nmi transpoz\u00e1zy podobn\u00fdmi Tn7. \u010ealej, d\u00f4kazy nazna\u010duj\u00fa, \u017ee V. parahaemolyticus z\u00edskal trh (hemolyz\u00edn s\u00favisiaci s TDH) od V. alginolyticus v pr\u00edpade HGT (Gonz\u00e1lez-Escalona et al, 2006; Xie et al, 2005). HGT bol identifikovan\u00fd ako pr\u00ed\u010dina vzniku patog\u00e9nnych klonov V. parahaemolyticus z prostredia.<\/p>\n\n\n\n H. pylori<\/em><\/strong> <\/p>\n\n\n\n H. pylori je mikroaerofiln\u00e1 gramnegat\u00edvna \u0161pir\u00e1lovit\u00e1 bakt\u00e9ria patriaca do kme\u0148a Campylobacterota, Proteobacteria. T\u00e1to bakt\u00e9ria sa nach\u00e1dza v hlienu, ktor\u00fd kolonizuje epitel \u017eal\u00fadka u viac ako 50 % svetovej popul\u00e1cie (Bravo et al., 2018; Proen\u00e7a-Modena et al., 2009). Z\u00e1va\u017enos\u0165 ochorenia z\u00e1vis\u00ed hlavne od faktorov hostite\u013ea a bakteri\u00e1lnych faktorov. Vo v\u00e4\u010d\u0161ine pr\u00edpadov je infekcia bezpr\u00edznakov\u00e1, ale ob\u010das sa m\u00f4\u017ee vyvin\u00fa\u0165 do peptick\u00fdch vredov, lymf\u00f3mu sliznicov\u00e9ho lymfatick\u00e9ho tkaniva a dokonca aj rakoviny \u017eal\u00fadka (GC). V roku 1994 bola H. pylori Svetovou zdravotn\u00edckou organiz\u00e1ciou zaraden\u00e1 do kateg\u00f3rie karcinog\u00e9nov triedy I (\u201eSchistosomes, liver flukes and Helicobacter pylori (1994). Pracovn\u00e1 skupina IARC pre hodnotenie karcinog\u00e9nnych riz\u00edk pre \u013eud\u00ed. Lyon, 7. \u2013 14. j\u00fan 1994\u201c). H. pylori s\u00fa \u0161pir\u00e1lovit\u00e9, ty\u010dinkovit\u00e9, zakriven\u00e9 bakt\u00e9rie s bi\u010d\u00edkmi a vonkaj\u0161\u00edm membr\u00e1nov\u00fdm obalom. Pohyblivos\u0165 je \u010fal\u0161ou d\u00f4le\u017eitou zlo\u017ekou ich patogenity, ktor\u00e1 umo\u017e\u0148uje bakt\u00e9ri\u00e1m prech\u00e1dza\u0165 muk\u00f3zovou vrstvou \u017eal\u00fado\u010dn\u00e9ho epitelu (Josenhans a Suerbaum, 2002). Akon\u00e1hle sa bakt\u00e9ria pripoj\u00ed k \u017eal\u00fado\u010dn\u00fdm epitelov\u00fdm bunk\u00e1m, sp\u00f4sobuje vakuoliz\u00e1ciu epitelov\u00fdch buniek, \u010do vedie k po\u0161kodeniu buniek. T\u00e1to vakuoliz\u00e1cia je v\u00fdsledkom produkcie cytotox\u00ednu naz\u00fdvan\u00e9ho vakuolizuj\u00faci cytotox\u00edn A (VacA), p\u00f3rovit\u00e9ho sekr\u00e9tneho tox\u00ednu, ktor\u00fd je zodpovedn\u00fd za rozsiahlu vakuoliz\u00e1ciu epitelov\u00fdch buniek, smr\u0165 buniek a naru\u0161enie integrity epitelu (Szab\u00f2 et al., 1999). Vakuoliz\u00e1cia sa m\u00f4\u017ee v\u00fdrazne l\u00ed\u0161i\u0165 od kme\u0148a ku kme\u0148u a existuje korel\u00e1cia medzi z\u00e1va\u017enos\u0165ou patogen\u00e9zy H. pylori a existenciou ostrova patogenity g\u00e9nu asociovan\u00e9ho s cytotox\u00ednom (PAI). D\u00f4le\u017eit\u00fdm faktorom virulencie je cagA, ktor\u00fd je pr\u00edtomn\u00fd v ostrove pribli\u017ene 30 g\u00e9nov, ktor\u00e9 H. pylori s najv\u00e4\u010d\u0161ou pravdepodobnos\u0165ou z\u00edskal od in\u00fdch organizmov. Klinicky v\u00fdznamn\u00fd H. pylori bol rozdelen\u00fd na kmene typu I a typu II. V\u0161etky kmene typu I maj\u00fa g\u00e9ny, ktor\u00e9 m\u00f4\u017eu produkova\u0165 cytotox\u00edny CagA aj VacA, zatia\u013e \u010do kmene typu II maj\u00fa len g\u00e9ny, ktor\u00e9 s\u00fa potrebn\u00e9 na produkciu VacA. H. pylori m\u00e1 pomerne zlo\u017eit\u00fa patofyziol\u00f3giu. V gen\u00f3me H. pylori sa nach\u00e1dza nieko\u013eko MGE a viacer\u00e9 \u0161t\u00fadie uv\u00e1dzaj\u00fa, \u017ee v gen\u00f3me patog\u00e9nu do\u0161lo k genetickej reorganiz\u00e1cii, ktor\u00e1 mu pom\u00e1ha prisp\u00f4sobi\u0165 sa drsn\u00fdm podmienkam v \u017eal\u00fadku a tie\u017e exprimova\u0165 g\u00e9ny virulencie a rezistencie. Ned\u00e1vna \u0161t\u00fadia uv\u00e1dza, \u017ee ICE typu \u0161tyri sekre\u010dn\u00e9ho syst\u00e9mu H. pylori (ICEHptfs) s\u00fa konzervovanou gen\u00f3movou oblas\u0165ou v H. pylori. Hoci bola t\u00e1to oblas\u0165 identifikovan\u00e1 ako konzervovan\u00e1, bolo zaznamenan\u00e9, \u017ee sa m\u00f4\u017ee mobilizova\u0165 prostredn\u00edctvom konjug\u00e1cie. Okrem toho t\u00e1to oblas\u0165 vykazovala vysok\u00fa diverzitu aliel. ICE prvok bol identifikovan\u00fd ako nosite\u013e g\u00e9nov, ktor\u00e9 k\u00f3duj\u00fa sekre\u010dn\u00fd syst\u00e9m typu 4 (T4SS), g\u00e9ny VirB, D a C. Okrem ICE v gen\u00f3me H. pylori je tento patog\u00e9n zn\u00e1my aj t\u00fdm, \u017ee obsahuje kryptick\u00e9 plazmidy, ktor\u00e9 poskytuj\u00fa oblasti, ktor\u00e9 s\u00fa hor\u00facimi bodmi pre \u0161pecifick\u00fa rekombin\u00e1ciu. Zauj\u00edmav\u00e9 je, \u017ee tento patog\u00e9n obsahuje aj plazmidy, ktor\u00e9 vykazuj\u00fa homol\u00f3giu s plazmidmi grampozit\u00edvnych organizmov, ktor\u00e9 sa replikuj\u00fa prostredn\u00edctvom mechanizmu rolling circle, a tie\u017e plazmidy, ktor\u00e9 sa replikuj\u00fa prostredn\u00edctvom mechanizmu theta. Okrem toho bolo v H. pylori identifikovan\u00fdch nieko\u013eko IS elementov, ktor\u00e9 obsahuj\u00fa g\u00e9ny vykazuj\u00face homol\u00f3giu s g\u00e9nmi in\u00fdch patog\u00e9nov, ako s\u00fa Salmonella (virulentn\u00fd g\u00e9n gipA) a E. coli (Vale et al., 2008).<\/p>\n\n\n\n In\u00e9 \u010drevn\u00e9 patog\u00e9ny<\/em><\/strong> <\/p>\n\n\n\n Odhaduje sa, \u017ee polovica v\u0161etk\u00fdch hna\u010dkov\u00fdch ochoren\u00ed je sp\u00f4soben\u00e1 \u010drevn\u00fdmi gramnegat\u00edvnymi bakt\u00e9riami. Tieto bakt\u00e9rie sa podie\u013eaj\u00fa na v\u00fdznamnej \u010dasti pr\u00edpadov hna\u010dky a \u010drevnej hor\u00fa\u010dky, ktor\u00e9 ro\u010dne sp\u00f4sobuj\u00fa viac ako tri mili\u00f3ny \u00famrt\u00ed. Hlavnou pr\u00ed\u010dinou hna\u010dkov\u00fdch infekci\u00ed je produkcia jedn\u00e9ho alebo viacer\u00fdch bakteri\u00e1lnych enterotox\u00ednov. \u010eal\u0161\u00edmi d\u00f4le\u017eit\u00fdmi \u010drevn\u00fdmi patog\u00e9nmi patriacimi do kme\u0148a Proteobacteria, Pseudomonadota s\u00fa V. cholerae a E. coli. V. cholerae sa sp\u00e1ja s jednou z najz\u00e1va\u017enej\u0161\u00edch hna\u010dkov\u00fdch infekci\u00ed, cholerou, zatia\u013e \u010do infekcie sp\u00f4soben\u00e9 enterotoxig\u00e9nnym E. coli (ETEC) s\u00fa zodpovedn\u00e9 za najv\u00e4\u010d\u0161\u00ed po\u010det pr\u00edpadov cestovate\u013eskej hna\u010dky. Medzi \u010fal\u0161ie d\u00f4le\u017eit\u00e9 gastrointestin\u00e1lne hna\u010dkov\u00e9 ochorenia sp\u00f4soben\u00e9 \u010drevn\u00fdmi patog\u00e9nmi patria Shigella spp., ktor\u00e9 patria do kme\u0148a Pseudomonadota, Proteobacteria, a Campylobacter jejuni, ktor\u00fd patr\u00ed do kme\u0148a Campylobacterota, Proteobacteria. Zo v\u00edrusov je zn\u00e1me, \u017ee rotav\u00edrus sp\u00f4sobuje najz\u00e1va\u017enej\u0161ie hna\u010dkov\u00e9 ochorenia u det\u00ed vo veku do 2\u20133 rokov. \u010eal\u0161\u00edmi v\u00fdznamn\u00fdmi gastrointestin\u00e1lnymi v\u00edrusmi s\u00fa kaliciv\u00edrusy a niektor\u00e9 druhy adenov\u00edrusov. Parazitick\u00e9 enterick\u00e9 patog\u00e9ny tie\u017e sp\u00f4sobuj\u00fa pr\u00edpady hna\u010dky, medzi ktor\u00e9 patria Entamoeba histolytica, Giardia lamblia a Cryptosporidium spp. Tieto patog\u00e9ny sp\u00f4sobuj\u00fa infekcie r\u00f4znymi sp\u00f4sobmi. Vo v\u0161eobecnosti zah\u0155\u0148a konven\u010dn\u00fd infek\u010dn\u00fd cyklus (1) vstup patog\u00e9nu, (2) usadenie a rast patog\u00e9nov vo vn\u00fatri hostite\u013eskej bunky, (3) ob\u00eddenie obranyschopnosti hostite\u013ea a (4) po\u0161kodenie hostite\u013ea a v\u00fdstup. V\u00e4\u010d\u0161ina t\u00fdchto funkci\u00ed je dosiahnut\u00e1 \u010drevn\u00fdmi patog\u00e9nmi s pomocou r\u00f4znych efektorov\u00fdch molek\u00fal. Efektorov\u00e9 molekuly mo\u017eno vo v\u0161eobecnosti klasifikova\u0165 ako tie, ktor\u00e9 pom\u00e1haj\u00fa bakt\u00e9ri\u00e1m pri koloniz\u00e1cii a usadzovan\u00ed sa patog\u00e9nu v \u010dreve hostite\u013ea, a tie, ktor\u00e9 pom\u00e1haj\u00fa patog\u00e9nu pri prenosu, ktor\u00fd je dosiahnut\u00fd po\u0161koden\u00edm buniek hostite\u013ea. Patog\u00e9n tie\u017e produkuje efektorov\u00e9 molekuly, ktor\u00e9 mu pom\u00e1haj\u00fa vyhn\u00fa\u0165 sa imunitn\u00e9mu syst\u00e9mu hostite\u013ea. Enterotox\u00edn, ktor\u00fd produkuj\u00fa kmene ETEC, je podobn\u00fd chol\u00e9rnemu tox\u00ednu (CT) a chol\u00e9ra aj hna\u010dka sp\u00f4soben\u00e1 ETEC ved\u00fa k ve\u013ekej strate vody a elektrolytov, ktor\u00e9 sa vylu\u010duj\u00fa v hornej p\u00e4tine tenk\u00e9ho \u010dreva. Infekcia ETEC vy\u017eaduje najsk\u00f4r adh\u00e9ziu a potom synt\u00e9zu tox\u00ednov. ETEC produkuje dva druhy enterotox\u00ednov, 84-kd tepelne labiln\u00fd tox\u00edn (LT) a druh\u00fd ETEC tox\u00edn, ktor\u00fd je tepelne stabiln\u00fd (ST) STa a STb. ST m\u00e1 teplotn\u00fa toleranciu 100 \u00b0C a iba STa, peptid s ve\u013ekos\u0165ou okolo 2 kD, bol spojen\u00fd s ochoren\u00edm \u013eud\u00ed (Joffr\u00e9 et al., 2016). Gen\u00f3my \u013eud\u00ed aj o\u0161\u00edpan\u00fdch maj\u00fa \u0161irok\u00fa \u0161k\u00e1lu g\u00e9nov, ktor\u00e9 k\u00f3duj\u00fa r\u00f4zne vari\u00e1cie LT. Varianty tepelne labiln\u00e9ho enterotox\u00ednu (LT) LTIp, LTIh, LTIc a LTIIa, k\u00f3dovan\u00e9 g\u00e9nom eltAB, s\u00fa pod\u013ea spr\u00e1v spojen\u00e9 s plazmidmi, chromoz\u00f3mami a prof\u00e1gmi (Jobling et al., 2012, 2016; Lasaro et al., 2008), zatia\u013e \u010do v\u00e4\u010d\u0161ina tepelne stabiln\u00fdch variantov tox\u00ednu u \u013eud\u00ed a o\u0161\u00edpan\u00fdch s\u00favis\u00ed s plazmidmi (Joffr\u00e9 et al., 2016; Taillon et al., 2008). ETEC aj V. cholerae maj\u00fa porovnate\u013en\u00e9 fimbrie, ktor\u00e9 s\u00fa k\u013e\u00fa\u010dov\u00e9 pre adh\u00e9ziu a koloniz\u00e1ciu bakt\u00e9ri\u00ed v tenkom \u010dreve hostite\u013ea. Koloniza\u010dn\u00e9 faktory, ktor\u00e9 s\u00fa k\u00f3dovan\u00e9 na plazmidoch, hraj\u00fa podstatn\u00fa \u00falohu pri sprostredkovan\u00ed adh\u00e9zie, zatia\u013e \u010do molekula adhez\u00ednu vonkaj\u0161ej membr\u00e1ny je \u010fal\u0161\u00edm d\u00f4le\u017eit\u00fdm faktorom virulencie, k\u00f3dovan\u00fdm v patog\u00e9nnom ostrove (Fleckenstein, et al., 1996). Okrem kontrastov existuj\u00fa aj podobnosti. Sekr\u00e9cia tekut\u00edn pri cholere je z ve\u013ekej \u010dasti, hoci nie v\u00fdlu\u010dne, sp\u00f4soben\u00e1 jedin\u00fdm enterotox\u00ednom. Ale enterotox\u00edny LT (tepelne labiln\u00fd tox\u00edn) a ST (tepelne stabiln\u00fd tox\u00edn) s\u00fa jedn\u00fdm alebo oboma, ktor\u00e9 vyvol\u00e1vaj\u00fa ak\u00fatne toxick\u00e9 hna\u010dkov\u00e9 ochorenia. G\u00e9ny CT s\u00fa k\u00f3dovan\u00e9 prof\u00e1gom (CT f\u00e1gom) umiestnen\u00fdm v chromoz\u00f3me, zatia\u013e \u010do v pr\u00edpade ETEC sa g\u00e9ny ST aj LT nach\u00e1dzaj\u00fa na plazmidoch a nie s\u00fa spojen\u00e9 s f\u00e1gom. V\u00e4\u010d\u0161ina gastrointestin\u00e1lnych patog\u00e9nov, vr\u00e1tane EPEC, Salmonella Shigella a Yersinia, pou\u017e\u00edva svoj T3SS na dod\u00e1vanie efektorov\u00fdch prote\u00ednov do hostite\u013esk\u00fdch buniek. Shigella \u013eahko napad\u00e1 epitelov\u00e9 bunky \u013eudsk\u00e9ho \u010dreva z bazolater\u00e1lnej plochy. Shigella sp. obsahuje jedin\u00fd kruhov\u00fd chromoz\u00f3m a avirulentn\u00fd plazmid. Virulentn\u00fd plazmid je sp\u00e1jan\u00fd s virulenciou a patogen\u00e9zou patog\u00e9nu. V\u00e4\u010d\u0161ina virulentn\u00fdch faktorov Shigella sa nach\u00e1dza v 30 kb oblasti naz\u00fdvanej \u201evstupn\u00e1 oblas\u0165\u201c, ktor\u00e1 obsahuje mxi-spa lokus, ktor\u00fd k\u00f3duje T3SS. Tento ve\u013ek\u00fd plazmid tie\u017e k\u00f3duje prote\u00edny (IpaB a IpaC), ktor\u00e9 pom\u00e1haj\u00fa bakt\u00e9ri\u00e1m vst\u00fapi\u0165 do hostite\u013esk\u00fdch buniek, mno\u017ei\u0165 sa a \u0161\u00edri\u0165 sa do susedn\u00fdch buniek (Sansonetti et al., 1999). Okrem virulentn\u00e9ho plazmidu obsahuj\u00fa patog\u00e9nne ostrovy (PAI) na chromoz\u00f3me Shigella aj g\u00e9ny, ktor\u00e9 prispievaj\u00fa k virulencii patog\u00e9nu. Zauj\u00edmav\u00e9 je, \u017ee bolo zisten\u00e9, \u017ee g\u00e9ny a in\u00e9 prvky v PAI sa m\u00f4\u017eu vyskytova\u0165 v r\u00f4znych kombin\u00e1ci\u00e1ch v z\u00e1vislosti od druhu a podtypu Shigella. Kombin\u00e1cia chromoz\u00f3mov\u00fdch virulentn\u00fdch faktorov a plazmidov\u00fdch virulentn\u00fdch faktorov sprostredkov\u00e1va invaz\u00edvnos\u0165 a virulenciu patog\u00e9nu. Shigella enterotox\u00edn 1 (ShET1) a Shigella enterotox\u00edn 2 (ShET2) s\u00fa hlavn\u00fdmi virulentn\u00fdmi faktormi, ktor\u00e9 sprostredkov\u00e1vaj\u00fa skor\u00fa sekr\u00e9ciu tekutiny v jejune a n\u00e1sledne v hrubom \u010dreve. ShET1 je k\u00f3dovan\u00fd g\u00e9nmi set1A a set1B na chromoz\u00f3me Shigella ako s\u00fa\u010das\u0165 PAI SHI-1. PAI je \u0161pecifick\u00fd iba pre izol\u00e1ty S. flexneri 2a (Vargas et al., 1999; Yavzori et al., 2002). Dve tox\u00ednov\u00e9 podjednotky spolu tvoria tox\u00ednov\u00fd komplex typu holo-AB v konfigur\u00e1cii A1-B5, podobn\u00fd cholera holotox\u00ednu, a s\u00fa sekr\u00e9tovan\u00e9 prostredn\u00edctvom Sec dr\u00e1hy a sekr\u00e9cie typu II (Faherty et al., 2012). \u010eal\u0161\u00edm v\u00fdznamn\u00fdm \u010drevn\u00fdm patog\u00e9nom je Yersinia, op\u00e4\u0165 \u010dlen kme\u0148a Pseudomonadota, Proteo bakt\u00e9rie, a tri druhy, a to Y. pestis, Y. enterocolitica a Y. pseudotuberculosis, s\u00fa zn\u00e1me t\u00fdm, \u017ee sp\u00f4sobuj\u00fa smrte\u013en\u00e9 ochorenia u \u013eud\u00ed. Tento patog\u00e9n je sp\u00e1jan\u00fd s infekciami region\u00e1lnych lymfatick\u00fdch uzl\u00edn alebo p\u013e\u00fac a tie\u017e s \u0161irokou \u0161k\u00e1lou gastrointestin\u00e1lnych ochoren\u00ed, od enterit\u00eddy po mezenterick\u00fa lymfadenit\u00eddu (Bibikova, 1977; Putzker et al., 2001; (Pujol a Bliska, 2005). Virulentn\u00e9 druhy Yersinia maj\u00fa nieko\u013eko virulentn\u00fdch faktorov, ako napr\u00edklad 70-kb virulentn\u00fd plazmid, pCD1 v Y. pestis a pYV v enteropatog\u00e9nnej Yersinia. Tie\u017e k\u00f3duj\u00fa syst\u00e9m yersiniabakt\u00ednu (Ybt) (Brubaker, 1991; Cornelis et al., 1998; Heesemann et al., 1993). Bolo zisten\u00e9, \u017ee 70-kb virulentn\u00fd plazmid v Y. pestis obsahuje nieko\u013eko g\u00e9nov, ktor\u00e9 k\u00f3duj\u00fa \u0161truktur\u00e1lne komponenty T3SS, ako aj efektorov\u00e9 prote\u00edny T3SS naz\u00fdvan\u00e9 vonkaj\u0161ie prote\u00edny Yersinia (Yops) (Bliska et al., 2013; Schwiesow et al., 2015). Je zn\u00e1me, \u017ee prote\u00edn Yops pom\u00e1ha patog\u00e9nu vyhn\u00fa\u0165 sa imunitn\u00e9mu syst\u00e9mu. Druhy Yersinia maj\u00fa tie\u017e nieko\u013eko T6SS s odli\u0161n\u00fdmi biologick\u00fdmi funkciami. T6SS dod\u00e1va viacero efektorov\u00fdch prote\u00ednov, zatia\u013e \u010do in\u00e9 sekre\u010dn\u00e9 syst\u00e9my dod\u00e1vaj\u00fa len jeden typ efektorov\u00e9ho prote\u00ednu. Okrem efektorov\u00fdch prote\u00ednov, ktor\u00e9 s\u00fa tox\u00ednmi, niektor\u00e9 efektorov\u00e9 molekuly dod\u00e1van\u00e9 prostredn\u00edctvom syst\u00e9mu T6SS tie\u017e zvy\u0161uj\u00fa perzistenciu patog\u00e9nu. T6SS m\u00e1 tie\u017e \u00falohu pri tvorbe biofilmu bakt\u00e9ri\u00ed (Southey-Pillig et al., 2005). R\u00f4zne tox\u00ednov\u00e9 g\u00e9ny spojen\u00e9 s MGE v r\u00f4znych bakteri\u00e1lnych enterick\u00fdch patog\u00e9noch s\u00fa zhrnut\u00e9 v tabu\u013eke 1.<\/p>\n\n\n\n Dynamika MGE spojen\u00fdch s tox\u00ednmi<\/em><\/strong> <\/p>\n\n\n\n Ako bolo uveden\u00e9 v predch\u00e1dzaj\u00facich \u010dastiach tohto preh\u013eadu, ve\u013ek\u00fd po\u010det determinantov virulencie bol spojen\u00fd s MGE u d\u00f4le\u017eit\u00fdch \u010drevn\u00fdch patog\u00e9nov. Hoci existuje nieko\u013eko \u0161t\u00fadi\u00ed a preh\u013eadov, ktor\u00e9 zd\u00f4raz\u0148uj\u00fa d\u00f4le\u017eitos\u0165 MGE spojen\u00fdch s ARG a ich dynamiku prenosu medzi komenz\u00e1lmi a patog\u00e9nmi, \u0161t\u00fadie zaoberaj\u00face sa d\u00f4le\u017eitos\u0165ou MGE spojen\u00fdch s g\u00e9nmi virulencie a ich dynamikou s\u00fa ojedinel\u00e9. Hoci sa HGT medzi druhmi z r\u00f4znych kme\u0148ov pova\u017euje za zriedkav\u00fd jav, v r\u00e1mci rovnak\u00e9ho druhu je be\u017en\u00fd. Existuj\u00fa v\u0161ak aj zauj\u00edmav\u00e9 spr\u00e1vy o HGT medzi r\u00f4znymi r\u00ed\u0161ami, kde bakteri\u00e1lne g\u00e9ny a ich prote\u00ednov\u00e9 homol\u00f3gy viedli k z\u00edskaniu funkci\u00ed v organizmoch vy\u0161\u0161ieho r\u00e1du, ako s\u00fa huby, nemat\u00f3dy a eukaryoty (Mayer et al., 2011; Moran a Jarvik, 2010). Jaramillo et al. (2015) identifikovali 11 pr\u00edpadov HGT toxick\u00fdch g\u00e9nov z bakt\u00e9ri\u00ed do rastlinn\u00fdch h\u00fab Colletotrichum gloeosporioides. Mnoh\u00e9 toxick\u00e9 g\u00e9ny homologick\u00e9 s g\u00e9nmi subtiliz\u00ednu z\u00edskali huby z Bacillus pumilus. \u010ealej existuj\u00fa aj spr\u00e1vy o dynamike kr\u00ed\u017eov\u00fdch kme\u0148ov tox\u00ednov s pozoruhodn\u00fdm pr\u00edkladom aerolyz\u00ednu, tox\u00ednu tvoriaceho p\u00f3ry pr\u00edtomn\u00e9ho v Aeromonas hydrophila, ktor\u00fd bol identifikovan\u00fd aj v mnoh\u00fdch patog\u00e9noch patriacich do kme\u0148ov Firmicutes a Proteobacteria (Kennedy et al., 2009). \u010ealej bolo pozorovan\u00e9, \u017ee MGE s \u0161irok\u00fdm spektrom hostite\u013eov prekra\u010duj\u00fa kmene a mobilizuj\u00fa sa z komenz\u00e1lov do izol\u00e1tov patog\u00e9nov (Forster et al., 2022). Forster a jeho t\u00edm porovnali viac ako 1000 gen\u00f3mov komenz\u00e1lnych kme\u0148ov patriacich k 540 druhom a viac ako 45 000 patog\u00e9nov patriacich k 12 druhom a zistili viac ako 64 000 pr\u00edpadov prenosu sprostredkovan\u00e9ho MGE medzi komenz\u00e1lmi a patog\u00e9nmi. Dobre presk\u00faman\u00fd prenos tox\u00ednov\u00e9ho g\u00e9nu v r\u00e1mci rovnak\u00e9ho bakteri\u00e1lneho druhu je prenos g\u00e9nu CT z toxig\u00e9nneho V. cholerae O1 do environment\u00e1lneho non-O1\/O139 V. cholerae (Choi et al., 2010). Vibrio f\u00e1gy, ktor\u00e9 s\u00fa be\u017en\u00fdmi obyvate\u013emi vodn\u00fdch syst\u00e9mov, s\u00fa zn\u00e1me t\u00fdm, \u017ee hraj\u00fa d\u00f4le\u017eit\u00fa \u00falohu v prenose g\u00e9nov CT (CTX-AB) z toxig\u00e9nneho kme\u0148a na netoxig\u00e9nny kme\u0148 a moduluj\u00fa dynamiku a evol\u00faciu V. cholerae. Transduk\u010dn\u00e9 experimenty boli vykonan\u00e9 s pou\u017eit\u00edm toxig\u00e9nnych kme\u0148ov V. cholerae O395 a E4 s cie\u013eom ur\u010di\u0165 schopnos\u0165 vibrio f\u00e1gov pren\u00e1\u0161a\u0165 g\u00e9ny CTX\u0278 do netoxig\u00e9nnych kme\u0148ov (Choi et al., 2010). Bolo zisten\u00e9, \u017ee NetB p\u00f3rovit\u00fd tox\u00edn produkovan\u00fd C. perfringens pri spolo\u010dnej kultiv\u00e1cii s izol\u00e1tmi C. perfringens negat\u00edvnymi na netB z\u00edskava g\u00e9n tox\u00ednu prostredn\u00edctvom prenosu konjugat\u00edvnej plazmidy pJIR3535 a pNetB-Ne10 (Lacey et al., 2017). \u010ealej, kr\u00ed\u017eov\u00fd HGT g\u00e9nov tox\u00ednov bol demon\u0161trovan\u00fd Muthukrishnanom et al. (2019) prostredn\u00edctvom experimentov so spolo\u010dnou kultiv\u00e1ciou izol\u00e1tov V. parahaemolyticus pozit\u00edvnych na pirAB a kme\u0148a Algoriphagus sp. negat\u00edvneho na pirAB. Prenos g\u00e9nu pirAB prebieha prostredn\u00edctvom konjugat\u00edvneho prenosu plazmidu pVA1. Tox\u00edn, ktor\u00fd sp\u00f4sobuje odlupovanie a degener\u00e1ciu hepatopankreasu kreviet, bol identifikovan\u00fd nielen vo V. parahaemolyticus, ale aj v nieko\u013ek\u00fdch \u010fal\u0161\u00edch Vibrio sp. a tie\u017e v ne-Vibrios (Dong et al., 2017; Restrepo et al., 2018). \u010eal\u0161\u00edm pr\u00edkladom prenosu g\u00e9nov tox\u00ednov medzi r\u00f4znymi druhmi bakt\u00e9ri\u00ed je konjugat\u00edvna plazm\u00edda (pVT1) V. tapetis, ktor\u00e1 sp\u00f4sobuje hned\u00e9 prstencov\u00e9 ochorenie. Je zn\u00e1me, \u017ee mozaikov\u00e1 plazm\u00edda obsahuje DNA regi\u00f3ny podobn\u00e9 t\u00fdm, ktor\u00e9 sa nach\u00e1dzaj\u00fa v V. vulnificus, Photobacterium profundum, Listonella anguillarum a Shewanella sp. Dynamika g\u00e9nov tox\u00ednov spojen\u00fdch s MGE medzi \u010drevn\u00fdmi patog\u00e9nmi a nepatog\u00e9nnymi bakt\u00e9riami sa m\u00f4\u017ee vyskytova\u0165 v \u010dreve, ale aj v prostred\u00ed. Je zn\u00e1me, \u017ee environment\u00e1lne parametre maj\u00fa v\u00fdznamn\u00fd vplyv na HGT a regul\u00e1ciu expresie g\u00e9nov virulencie. Je zn\u00e1me, \u017ee prostredie biofilmu zvy\u0161uje r\u00fdchlos\u0165 HGT v d\u00f4sledku tesnej bl\u00edzkosti bakteri\u00e1lnych buniek v biofilme (Gyles a Boerlin, 2013). Okrem toho je zn\u00e1me, \u017ee syst\u00e9my TA prispievaj\u00fa k selekcii a udr\u017eaniu MGE (Aminov et al., 2011). Syst\u00e9m TA pozost\u00e1va zo stabiln\u00e9ho tox\u00ednu pr\u00edtomn\u00e9ho v chromoz\u00f3me a labiln\u00e9ho antitox\u00ednu, ktor\u00fd sa zvy\u010dajne nach\u00e1dza na plazmidoch. Ke\u010f bakteri\u00e1lne bunky stratia plazmid, expresia antitox\u00ednu sa zastav\u00ed a expresia tox\u00ednu sp\u00f4sob\u00ed smr\u0165 buniek. Tento dvojzlo\u017ekov\u00fd syst\u00e9m tak selekt\u00edvne eliminuje bakteri\u00e1lne bunky bez plazmidov v popul\u00e1cii (Aminov et al., 2011). Preto pochopenie environment\u00e1lnych faktorov ovplyv\u0148uj\u00facich prenos, genetiku a dynamiku virulencie spojenej s MGE pom\u00f4\u017ee objasni\u0165 evol\u00faciu bakt\u00e9ri\u00ed a pochopi\u0165 futuristick\u00e9 vznikaj\u00face bakteri\u00e1lne patog\u00e9ny. \u010ealej, pochopenie \u0161irok\u00fdch hostite\u013esk\u00fdch MGE m\u00f4\u017ee umo\u017eni\u0165 v\u00fdskumn\u00edkom identifikova\u0165 pr\u00edrodn\u00e9 a syntetick\u00e9 molekuly, ktor\u00e9 m\u00f4\u017eu zn\u00ed\u017ei\u0165 ich mobilitu, \u010d\u00edm zabr\u00e1nia virulencii a prenosu ARG.<\/p>\n\n\n\n S\u00fahrn<\/em><\/strong> <\/p>\n\n\n\n Prerazenie v sekven\u010dn\u00fdch technol\u00f3gi\u00e1ch otvorilo dvere k sk\u00famaniu nespo\u010detn\u00e9ho mno\u017estva mikr\u00f3bov ob\u00fdvaj\u00facich \u013eudsk\u00e9 \u010drevo. Poznatky o ich gen\u00f3moch pomohli pochopi\u0165 ekol\u00f3giu r\u00f4znych mikr\u00f3bov, ich funkcie, ako aj dynamiku MGE spojen\u00fdch s r\u00f4znymi fitness vlastnos\u0165ami. U v\u00e4\u010d\u0161iny bakteri\u00e1lnych \u010drevn\u00fdch patog\u00e9nov je pr\u00ed\u010dinou ochorenia produkcia tox\u00ednov, ktor\u00e9 s\u00fa k\u00f3dovan\u00e9 t\u00fdmito MGE. Tieto MGE zah\u0155\u0148aj\u00fa najm\u00e4 f\u00e1gy, patog\u00e9nne ostrovy, plazmidy a transpoz\u00f3ny. V tejto \u0161t\u00fadii s\u00fa zhrnut\u00e9 r\u00f4zne MGE spojen\u00e9 s virulentn\u00fdmi vlastnos\u0165ami klinicky v\u00fdznamn\u00fdch \u010drevn\u00fdch patog\u00e9nov. \u010eal\u0161ie \u0161t\u00fadie o MGE pripravia p\u00f4du pre lep\u0161ie pochopenie ich bakteri\u00e1lnej \u0161pecificity, mechanizmov integr\u00e1cie a exc\u00edzie, ako aj dedi\u010dnosti. Toto pochopenie m\u00f4\u017ee \u010falej pom\u00f4c\u0165 v\u00fdskumn\u00edkom pri navrhovan\u00ed strat\u00e9gi\u00ed na prevenciu \u0161\u00edrenia t\u00fdchto MGE, ktor\u00e9 zohr\u00e1vaj\u00fa d\u00f4le\u017eit\u00fa \u00falohu pri zmier\u0148ovan\u00ed ochorenia. \u010ealej je mo\u017en\u00e9 formulova\u0165 r\u00f4zne strat\u00e9gie, ako napr\u00edklad skr\u00edning pr\u00edrodn\u00fdch a syntetick\u00fdch zl\u00fa\u010den\u00edn, ktor\u00e9 m\u00f4\u017eu vylie\u010di\u0165 MGE z bakteri\u00e1lnych patog\u00e9nov, \u010d\u00edm sa stan\u00fa menej virulentn\u00fdmi a citliv\u00fdmi na existuj\u00face antibiotik\u00e1. Tieto strat\u00e9gie, navrhnut\u00e9 na boj proti stabilite t\u00fdchto MGE, by mohli pom\u00f4c\u0165 zn\u00ed\u017ei\u0165 z\u00e1\u0165a\u017e ochoren\u00edm a zabr\u00e1ni\u0165 vzniku mutantov odoln\u00fdch vo\u010di antibiotik\u00e1m v bud\u00facnosti. <\/p>\n\n\n\n Po\u010fakovanie. \u010eakujeme Dr. G. Balakrishovi Nair za jeho cenn\u00e9 pripomienky. Pani Shashi Kumari \u010fakuje CSIR-GOI za jej doktorandsk\u00e9 \u0161tipendium. Dr. Deepjyoti Paul a Dr. Lekshmi N \u010fakuj\u00fa DBT-GOI za \u0161tipendijn\u00fd program MK Bhan. Pr\u00edspevok autorov. S.P., S.K. a B.D. vypracovali p\u00f4vodn\u00fa recenziu; J.V., S.B., D.P., L.N. a B.D. recenziu upravili a finalizovali. Financovanie. T\u00e1to \u0161t\u00fadia bola finan\u010dne podporen\u00e1 Ministerstvom biotechnol\u00f3gie (DBT) indickej vl\u00e1dy (grant \u010d. BT\/PR38173\/MED\/97\/474\/2020). <\/p>\n\n\n\n Konflikt z\u00e1ujmov. Autori vyhlasuj\u00fa, \u017ee neexistuje \u017eiadny konflikt z\u00e1ujmov. Pozn\u00e1mky o prispievate\u013eoch. SP, SK, JV, SB, LN a DP vytvorili prv\u00fd n\u00e1vrh recenzie. BD recenziu upravil a finalizoval.<\/p>\n\n\n\n References Brede DA, Snipen LG, Ussery DW, Nederbragt AJ and Nes IF (2011) Complete genome sequence of the commensal Daniels NA, MacKinnon L, Bishop R, Altekruse S, Ray B, Hammond RM, \u2026 Slutsker L (2000) Vibrio parahaemolyticus Franciosa G, Maugliani A, Scalfaro C, Aureli P (2009) Evidence that plasmid-borne botulinum neurotoxin type B genes are Jobling MG(2016)Thechromosomal nature ofLT-II enterotoxins solved: A lambdoid prophage encodes both LT-II and one Letchumanan V, Chan KG and Lee LH (2014) Vibrio parahaemolyticus: A review on the pathogenesis, prevalence, and Muthukrishnan S, Defoirdt T, Shariff M, Ina-Salwany MY, Yousoff FM andNatrah I(2019) Horizontal gene transfer of the Stevens RH,Ektefaie MRandFoutsDE(2011)TheannotatedcompleteDNAsequenceofEnterococcusfaecalisbacteriophage \u00a9 Autori, 2025. Publikovan\u00e9 Cambridge University Press v spolupr\u00e1ci s The Nutrition Society. Ide o \u010dl\u00e1nok s vo\u013en\u00fdm pr\u00edstupom, distribuovan\u00fd pod\u013ea podmienok licencie Creative Commons Attribution (http:\/\/creativecommons.org\/licenses\/by\/4.0), ktor\u00e1 umo\u017e\u0148uje neobmedzen\u00e9 op\u00e4tovn\u00e9 pou\u017eitie, distrib\u00faciu a reprodukciu za predpokladu, \u017ee je spr\u00e1vne citovan\u00fd p\u00f4vodn\u00fd \u010dl\u00e1nok.<\/p>\n","protected":false},"excerpt":{"rendered":" V tomto \u010dl\u00e1nku se jedn\u00e1 se o zji\u0161t\u011bn\u00ed z nov\u00e9 studie publikovan\u00e9 na Cambridge university. Origin\u00e1l \u010dl\u00e1nku publikov\u00e1n online Cambridge University Press dne 24. \u00fanora 2023 Nejprve kr\u00e1tk\u00fd sum\u00e1\u0159. Sly\u0161eli jste u\u017e o st\u0159evn\u00edm mikrobiomu? Je to miliardov\u00e1 komunita, kter\u00e1 kontroluje va\u0161e\u2026<\/p>","protected":false},"author":2,"featured_media":17447,"comment_status":"closed","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[69],"tags":[229,226,227,230,228],"class_list":["post-17439","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-vedecke-studie-a-nove-zistenia","tag-horizontalny-prenos-genov","tag-mobilne-geneticke-prvky","tag-patogeny","tag-rezistencia-na-lieky","tag-toxiny"],"aioseo_notices":[],"_links":{"self":[{"href":"https:\/\/ziveprobiotika.sk\/cz\/wp-json\/wp\/v2\/posts\/17439","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/ziveprobiotika.sk\/cz\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/ziveprobiotika.sk\/cz\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/ziveprobiotika.sk\/cz\/wp-json\/wp\/v2\/users\/2"}],"replies":[{"embeddable":true,"href":"https:\/\/ziveprobiotika.sk\/cz\/wp-json\/wp\/v2\/comments?post=17439"}],"version-history":[{"count":0,"href":"https:\/\/ziveprobiotika.sk\/cz\/wp-json\/wp\/v2\/posts\/17439\/revisions"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/ziveprobiotika.sk\/cz\/wp-json\/wp\/v2\/media\/17447"}],"wp:attachment":[{"href":"https:\/\/ziveprobiotika.sk\/cz\/wp-json\/wp\/v2\/media?parent=17439"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/ziveprobiotika.sk\/cz\/wp-json\/wp\/v2\/categories?post=17439"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/ziveprobiotika.sk\/cz\/wp-json\/wp\/v2\/tags?post=17439"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}Tich\u00ed agenti: Mobiln\u00e9 genetick\u00e9 elementy<\/h3>\n\n\n\n
\n
Tox\u00edny ako dar\u010dek: Pr\u00edbehy z podsvetia<\/h3>\n\n\n\n
\u010co to znamen\u00e1 pre n\u00e1s?<\/h3>\n\n\n\n
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Functional GenomicsLaboratory,InfectionandImmunologyDivision,TranslationalHealthScienceandTechnologyInstitute,Faridabad, India *Corresponding author. Email: bhabatosh@thsti.res.in (Received 16 February 2022; revised 31 December 2022; accepted 24 February 2023)<\/p>\n\n\n\n![\"\"](\"https:\/\/ziveprobiotika.sk\/wp-content\/uploads\/2025\/10\/image-37.png\")
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vyskytuje preva\u017ene u \u201estudenokrvn\u00fdch\u201c zvierat, ako s\u00fa oboj\u017eiveln\u00edky, ryby a plazy, a je tie\u017e zn\u00e1me, \u017ee sp\u00f4sobuje menej ako 1 % infekci\u00ed u \u013eud\u00ed (Tomastikova et al., 2017). Salmonely s\u00fa z medic\u00ednskeho h\u013eadiska kategorizovan\u00e9 na tyfov\u00e9 (S. Paratyphi A, S. Paratyphi B, S. Typhi) a net\u00fdfov\u00e9 Salmonella (napr. Enteritidis). S. Typhi murium je zn\u00e1me t\u00fdm, \u017ee sp\u00f4sobuje t\u00fdfus, S. Paratyphi A, B a C sp\u00f4sobuj\u00fa \u010drevn\u00fa hor\u00fa\u010dku a in\u00e9 s\u00e9rotypy S. Paratyphi sp\u00f4sobuj\u00fa salmonel\u00f3zu. S\u00e9rovary Salmonella, o ktor\u00fdch je zn\u00e1me, \u017ee sp\u00f4sobuj\u00fa gastroenterit\u00eddu, sa m\u00f4\u017eu \u0161\u00edri\u0165 kontaminovan\u00fdmi potravinami alebo vodou alebo priamo fek\u00e1lno-or\u00e1lnou cestou. V\u00e4\u010d\u0161ina s\u00e9rotypov Salmonella m\u00f4\u017ee sp\u00f4sobi\u0165 gastroenterit\u00eddu, zatia\u013e \u010do mal\u00fd po\u010det, ako napr\u00edklad S.Typhi, m\u00f4\u017ee sp\u00f4sobi\u0165 invaz\u00edvnu infekciu (Rabsch et al., 2001). Patogenita infekci\u00ed Salmonella zah\u0155\u0148a rok\u00fa \u0161k\u00e1lu virulentn\u00fdch faktorov, ako s\u00fa patogenitn\u00e9 ostrovy Salmonella SPI-1, SPI-2 a in\u00e9 SPI, ktor\u00e9 s\u00fa k\u00f3dovan\u00e9 sekre\u010dn\u00fdmi syst\u00e9mami typu 3 (T3SS), ako aj bi\u010d\u00edky, kapsuly, plazmidy a adh\u00e9zne syst\u00e9my.
V\u00fdvoj T3SS-2 a intracelul\u00e1rna reprodukcia prebiehaj\u00fa v membr\u00e1nou ohrani\u010denom kompartmente
zn\u00e1mom ako vakuola obsahuj\u00faca Salmonella (SCV). Dva konzervovan\u00e9 a stabiln\u00e9 PAI, zn\u00e1me ako patog\u00e9nne ostrovy Salmonella 1 a 2 (SPI-1a SPI-2), s\u00fa pr\u00edtomn\u00e9 vo v\u0161etk\u00fdch druhoch S. enterica. SPI-1 exprimoval sekre\u010dn\u00fd syst\u00e9m typu 3 (TTSS-1), obsahuj\u00faci invaz\u00edvne g\u00e9ny, ktor\u00e9 umo\u017e\u0148uj\u00fa bakt\u00e9ri\u00e1m vst\u00fapi\u0165 do hostite\u013esk\u00fdch \u010drevn\u00fdch epiteli\u00e1lnych buniek prostredn\u00edctvom procesu zah\u0155\u0148aj\u00faceho polymeriz\u00e1ciu akt\u00ednu a remodel\u00e1ciu cytoskeletu (Raffatellu et al., 2005, Jajere 2019). Okrem toho sa SPI-2, k\u00f3dova\u010d TTSS-2, syntetizuje ke\u010f Salmonella infikuje fagocyt\u00e1rne bunky hostite\u013ea, ako s\u00fa dendritick\u00e9
bunky a makrof\u00e1gy, \u010do u\u013eah\u010duje pre\u017e\u00edvanie Salmonella vo vakuole zn\u00e1mej ako \u201eSCV\u201c t\u00fdm, \u017ee spoma\u013euje v\u00fdvoj vakuoly a jej f\u00faziu s lyzoz\u00f3mami. Prolifer\u00e1cia Salmonella v podmienkach s n\u00edzkymi hladinami hor\u010d\u00edka, ako napr\u00edklad v makrof\u00e1goch, z\u00e1vis\u00ed od SPI-3 (Amavisit et al., 2003, Foley et al., 2013). G\u00e9ny
nach\u00e1dzaj\u00face sa na SPI-4 s\u00fa nevyhnutn\u00e9 pre pre\u017eitie v makrof\u00e1goch, apopt\u00f3zu a uvo\u013e\u0148ovanie tox\u00ednov.
G\u00e9ny SPI-5 k\u00f3duj\u00fa r\u00f4zne efekt\u00edvne prote\u00edny T3SS, zatia\u013e \u010do g\u00e9ny k\u00f3dovan\u00e9 SPI-6 transportuj\u00fa prote\u00edny do bunkov\u00e9ho prostredia alebo hostite\u013esk\u00fdch buniek v reakcii na vonkaj\u0161ie podnety. Navy\u0161e, S. enterica subsp. enterica disponovala ve\u013ek\u00fdm excisovate\u013en\u00fdm PAI, ostrovom patogenity Salmonella 7 (SPI-7),
ktor\u00fd obsahoval pribli\u017ene 150 g\u00e9nov. SPI-7 m\u00e1 ve\u013ekos\u0165 pribli\u017ene 134 kb a obsah GC pribli\u017ene 49,7 %. SPI-7 bol identifikovan\u00fd ako vysoko mozaikov\u00fd a zd\u00e1 sa, \u017ee bol odvoden\u00fd postupn\u00fdm z\u00edskavan\u00edm r\u00f4znych
g\u00e9nov. Okrem g\u00e9nov, ktor\u00e9 sa podie\u013eaj\u00fa na jeho mobiliz\u00e1cii, bolo zisten\u00e9, \u017ee ostrov patogenity obsahuje aj virulentn\u00e9 g\u00e9ny, ako je Vi antig\u00e9n, SopE f\u00e1g a typ IVB pilus locus (Bueno et al., 2004). Virulentn\u00fd g\u00e9n sopE (STY4609) k\u00f3duje prote\u00edn SopE, efektorov\u00fd prote\u00edn uvo\u013e\u0148ovan\u00fd TTSS-1, ktor\u00fd sp\u00f4sobuje preskupenie akt\u00ednu v epitelov\u00fdch bunk\u00e1ch, bol identifikovan\u00fd ako s\u00fa\u010das\u0165 prof\u00e1gu podobn\u00e9ho P2 umiestnen\u00e9ho uprostred SPI-7. S. enterica serovar Enteritidis (S. enteritidis) je patog\u00e9nna bakt\u00e9ria, ktor\u00e1 m\u00e1 nestabiln\u00fd patog\u00e9nny ostrov s ve\u013ekos\u0165ou 26,5 kb naz\u00fdvan\u00fd Region of Difference 21 alebo ROD21 (SPI19). Ostrov patogenity ROD21 bol identifikovan\u00fd ako pr\u00edtomn\u00fd v chromoz\u00f3me S. enteritidis spojen\u00fd s radom g\u00e9nov virulencie (Pardo-Roa et al., 2019). Salmonella a r\u00f4zne odli\u0161n\u00e9 s\u00e9rotypy boli objavili, \u017ee obsahuj\u00fa teplotne z\u00e1visl\u00e9, diverzifikovan\u00e9 a hostite\u013esky obmedzen\u00e9 konjuga\u010dn\u00e9 plazmidy IncC, IncF, IncHI a IncI1, obsahuj\u00face g\u00e9ny AR. Konkr\u00e9tne, konjuga\u010dn\u00fd virulentn\u00fd plazmid IncF bol z\u00edskan\u00fd z vt\u00e1\u010dieho patog\u00e9nneho kme\u0148a E. coli (Lindsey et al., 2009).<\/p>\n\n\n\n![\"\"](\"https:\/\/ziveprobiotika.sk\/wp-content\/uploads\/2025\/10\/image-39.png\")
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