Helicobacter bills triggers persistent immune reactivily to antigens derived from the commensal bacteria in gnotobiotic C3H/HeN mice

Jergens, Albert E.; Wilson-Welder, Jennifer H.; Dorn, Andrea; Henderson, Abigail; Zhiping Liu; Evans, Richard B.; Hostetter, Jesse; Wannemuehler, Michael J.
July 2007
Gut;Jul2007, Vol. 56 Issue 7, p934
Academic Journal
Background: Infection with Helicobacter species has been associated with the development of mucosal inflammation and inflammatory bowel disease (IBD) in several mouse models. However, consensus regarding the role of Helicobacteras a model organism to study microbial-induced IBD is confounded by the presence of a complex colonic microbiota. Aim: To investigate the kinetics and inflammatory effects of immune system activation to commensal bacteria following H biffs colonisation in gnotobiotic mice. Methods: C3H/HeN mice harbouring an altered Schaedler flora (ASF) were selectively colonised with H biffs and host responses were investigated over a 10-week period. Control mice were colonised only with the defined flora (DF). Tissues were analysed for gross/histopathological lesions, and bacterial antigen-specific antibody and T-cell responses. Results: Gnotobiotic mice colonised with H biffs developed mild macroscopic and microscopic lesions of typhlocolitis beginning 3 weeks postinfection. ASF-specific IgG responses were demonstrable within 3 weeks, persisted throughout the 10-week study, and presented as a mixed IgGl:lgG2a profile. Lymphocytes recovered from the mesenteric lymph node of H bilis-colonised mice produced increased levels of interferon γ, tumour necrosis factor α (TNFα), interleukin 6 (IL6) and IL12 in response to stimulation with commensal- or H biffs-specific bacterial lysates. In contrast, DF mice not colonised with H biffs did not develop immune responses to their resident flora and remained disease free. Conclusions: Colonisation of gnotobiotic C3H/HeN mice with H bilis perturbs the host's response to its resident flora and induces progressive immune reactivily to commensal bacteria that contributes to the development of immune-mediated intestinal inflammation.


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