Germ-free mice do not develop ankylosing enthesopathy, a spontaneous joint disease
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu srovnávací studie, časopisecké články, práce podpořená grantem
PubMed
10825583
DOI
10.1016/s0198-8859(00)00122-1
PII: S0198-8859(00)00122-1
Knihovny.cz E-zdroje
- MeSH
- ankylózující spondylitida mikrobiologie MeSH
- gnotobiologické modely * MeSH
- incidence MeSH
- modely nemocí na zvířatech MeSH
- myši MeSH
- nemoci kloubů epidemiologie mikrobiologie MeSH
- revmatické nemoci epidemiologie mikrobiologie MeSH
- revmatoidní artritida mikrobiologie MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- srovnávací studie MeSH
Ankylosing enthesopathy (ANKENT) is a naturally occurring joint disease in mice with numerous parallels to human ankylosing spondylitis (AS). Similarities between AS and ANKENT include not only affected tissue (joint entheses) but also association of the disease with genetic background, including MHC genes, gender, and age. Young males with the C57Bl/10 background have been described to suffer from ANKENT and, among H-2 congenic strains, high frequency of afflicted joints has been recorded in B10.BR (H-2(k)) males. Interestingly, the incidence of ANKENT is higher in conventional (CV) males that in their specific-pathogen-free (SPF) counterparts. The latter finding suggests that microbes could play a role as an ANKENT-triggering agent. To further examine this hypothesis we have established a germ-free (GF) colony of B10.BR mice and observed ANKENT incidence in both GF males and their conventionalized (ex-GF) male littermates; 20% of ex-GF males developed ANKENT before 1 year of age. In contrast, no joint disease was observed under GF conditions (p < 0.0001). Our results show that live microflora is required in ANKENT pathogenesis.
Citace poskytuje Crossref.org
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