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 Helicobacter as 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. bilis colonization in gnotobiotic mice.
Methods: C3H/HeN mice harboring an altered Schaedler flora were selectively colonized with H. bilis and host responses were investigated over a 10 week period. Control mice were colonized only with the defined flora. Tissues were analyzed for gross/histopathologic lesions and bacterial antigen-specific antibody and T cell responses.
Results: Gnotobiotic mice colonized with H. bilis developed mild macro- and microscopic lesions of typhlocolitis beginning 3 weeks post-infection. ASF-specific IgG responses were demonstrable within 3 weeks, persisted throughout the 10 week study, and presented as a mixed IgG1:IgG2a profile. Lymphocytes recovered from the mesenteric lymph node of H. bilis-colonized mice produced increased levels of IFN-γ, TNF-α, IL-6, and IL-12 in response to stimulation with commensal- or H. bilis-specific bacterial lysates. In contrast, defined flora mice not colonized with H. bilis did not develop immune responses to their resident flora and remained disease free.
Conclusions: Colonization of gnotobiotic C3H/HeN mice with H. bilis perturbs the host's response to its resident flora and induces progressive immune reactivity to commensal bacteria that contributes to the development of immune-mediated intestinal inflammation.
- altered Schaedler flora
- bacterial provocateur
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