Different subsets of enteric bacteria induce and perpetuate experimental colitis in rats and mice

Citation
Hc. Rath et al., Different subsets of enteric bacteria induce and perpetuate experimental colitis in rats and mice, INFEC IMMUN, 69(4), 2001, pp. 2277-2285
Citations number
52
Categorie Soggetti
Immunology
Journal title
INFECTION AND IMMUNITY
ISSN journal
00199567 → ACNP
Volume
69
Issue
4
Year of publication
2001
Pages
2277 - 2285
Database
ISI
SICI code
0019-9567(200104)69:4<2277:DSOEBI>2.0.ZU;2-D
Abstract
Resident bacteria are incriminated in the pathogenesis of experimental coli tis and inflammatory bowel diseases. We investigated the relative roles of various enteric bacteria populations in the induction and perpetuation of e xperimental colitis. HLA-B27 transgenic rats received antibiotics (ciproflo xacin, metronidazole, or vancomycin-imipenem) in drinking water or water al one in either prevention or treatment protocols. Mice were treated similarl y with metronidazole or vancomycin-imipenem before or after receiving 5% de xtran sodium sulfate (DSS). Germfree transgenic rats were colonized with sp ecific-pathogen-free enteric bacteria grown overnight either in anaerobic o r aerobic atmospheres. Nontransgenic rats colonized with anaerobic bacteria served as negative controls. Although preventive metronidazole significant ly attenuated colitis in transgenic rats and DSS-treated mice, it had no th erapeutic benefit once colitis was established. Ciprofloxacin also partiall y prevented but did not treat colitis in B27 transgenic rats. In both anima l models vancomycin-imipenem most effectively prevented and treated colitis . Germfree transgenic rats reconstituted with enteric bacteria grown under anaerobic conditions had more aggressive colitis than those associated with aerobic bacteria. These results suggest that a subset of resident luminal bacteria induces colitis, but that a complex interaction of commensal aerob ic and anaerobic bacteria provides the constant antigenic drive for chronic immune-mediated colonic inflammation.