Joint disease ankylosing enthesopathy (ANKENT) naturally occurs in inbred mice with C57Bl/10 genetic background. ANKENT has many parallels to human ankylosing spondylitis (AS) and represents an animal model for AS. Environmental conditions (i.e., microbial load of the organism) are among the risk factors for ANKENT, similar to AS. The role of microflora in the development of ANKENT was investigated. ANKENT was tested in four experimental groups of germ-free mice associated with different numbers of various intestinal microbes and three control groups: germ-free, specific pathogen-free, and conventional (CV) mice. Mice were colonized either with anaerobic bacteria isolated from the intestine of a CV mouse or with bacterial strains obtained from the collection of microorganisms. Microbes were characterized and checked by microbiological cultivation methods and with the use of polymerase chain reaction amplification and rDNA sequence analysis. Joint disease developed in GF mice colonized with a mixture containing Bacteroides spp. and Enterococcus sp., and/or Veillonella sp. and Staphylococcus sp. No ANKENT appeared in males colonized with probiotic bacterium Lactobacillus sp. In control groups ANKENT occurred in SPF and CV animals; the GF animals remained healthy. The results confirmed that the germ-free conditions protect from joint inflammation, and thus microbes are necessary for ANKENT development. In colonized mice the ANKENT was triggered by luminal anaerobic bacteria, which are common components of intestinal microflora.
- MeSH
- ankylózující spondylitida imunologie mikrobiologie MeSH
- DNA bakterií analýza MeSH
- druhová specificita MeSH
- grampozitivní bakteriální infekce imunologie MeSH
- grampozitivní bakterie genetika imunologie izolace a purifikace patogenita MeSH
- myši inbrední C57BL MeSH
- myši MeSH
- organismy bez specifických patogenů MeSH
- polymerázová řetězová reakce MeSH
- rizikové faktory MeSH
- sekvenční analýza DNA MeSH
- slizniční imunita imunologie MeSH
- střevní nádory imunologie mikrobiologie MeSH
- stupeň závažnosti nemoci MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- práce podpořená grantem MeSH
Článok sa zaoberá novým pohľadom na možnú spolulúčasť E. coli v patogenéze zápalových ochorení čriev. Pri vzniku zápalovej reakcie v čreve sa ako jeden z možných etiologických agensov uplatňujú baktérie, najmä oportúnne. E. coli je dominantným mikroorganizmom pri vzniku skorých a chronických lézií ilea pri Crohnovej chorobe, ulceróznej kolitíde a kolorektálnom karcinóme. Kmene E. coli, izolované z bioptických vzoriek čreva pacientov so zápalovými a nádorovými ochoreniami čriev, sú často asociované s mukózou čreva a vyznačujú sa schopnosťou adherovať a invadovať epitelové bunky čreva in vitro. Táto potenciálne patogénna skupina invazívnych E. coli bola označená ako adherentno-invazívne E. coli. Mechanizmus ich patogenézy spočíva v adherencii k črevným epitelovým bunkám a následnej kolinizácii mukózy čreva. Kolonizáciu umožňujú povrchové adhezíny baktérií, najmä fimbrie typu 1 a špecifické receptory na povrchu hostiteľských buniek. Kmene vstupujú do hostiteľských buniek spôsobom podobným makropinocytóze a množia sa v cytoplazme. Vyznačujú sa schopnosťou pomnožiť sa v makrofágoch bez toho, aby indukovali ich usmrtenie. Tento ivazívny proces adherentno-invazívnych E. coli je jedinečný, pretože neobsahujú žiadny zo známych genetických ivazívnych determinantov.
The article discusses a possible participation of E. coli in the pathogenesis of inflammatory bowel diseases. Bacteria, especially opportunistic, may play a role as one of the possible aetiologic agents in the initiation of the inflammatory reaction in the colon. E. coli is predominant microorganism in the initiation of early and chronic ileal lesions of Crohn disease, ulcerative colitis and colorectal carcinoma. E. coli strains isolated from biopsy specimens of colon of patients with inflammatory and tumor bowel diseases are often associated to mucosa of colon. They are able both to adhere and invade epithelial cells of colon in vitro. These strains belong to a potentially pathogenic group of invasive E. coli, which was designated as a group of adherent-invasive E. coli. Mechanism of their pathogenicity reflects their capability to adhere onto epithelial cells of colon and following mucosal colonisation. The colonisation is mediated by adhesins at the surface of the bacteria, especially type 1 pili and specific receptors at the surface of the host cells. E. coli strains enter the host cells using a way similar to macropinocytosis and multiply in the cytoplasm. They are able to replicate within macrophages without their killing. The invasive process of adherent-invasive E. coli is original, in that they possess none of the known genetic invasive determinants.
