English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Inflammatory bowel disease is a chronic inflammation of the gastrointestinal tract (GI) that develops in part as a result of an aberrant immune response to enteric bacteria in the GI tract. Prior studies indicate that Helicobacter bilis colonization of immune competent, defined-flora (DF) mice induced antigen-specific responses to their resident flora, in the absence of colitis. We hypothesize that H. bilis colonization of DF mice perturbs mucosal homeostasis and, thus, alters tolerance to the commensal flora and increases the host’s sensitivity to an inflammatory insult. Defined flora mice were colonized with Helicobacter bilis for up to 20 weeks prior to treatment with low-dose (1.5%) dextran sulfate sodium (DSS). Mice were evaluated for gross and histological lesions as well as cellular and humoral responses in comparison to controls. In comparison to DSS treated or H. bilis colonization alone, mice dually treated with H. bilis and DSS developed significantly (p < .05) increased gross and histopathological lesions including cecal atrophy, decreased colon length, and histological inflammation. Serum IgG2a responses to antigens derived from the enteric flora were increased compared to controls. Evaluation of the proximal colon indicated an increase in mucosal IL-17, IFN-γ, and TNF-α after colonization and/or DSS treatment. The magnitude of antigen-specific T cell proliferation increased with time, as Foxp3 expression declined; however, lesions did not increase in severity. Susceptibility to DSS-induced colitis was associated with increased antigen-specific reactivity to the enteric flora and mucosal expression of inflammatory cytokines. In conclusion, these studies demonstrate that perturbation of the microbial ecology following colonization with a mildly pathogenic bacteria, such as H. bilis, may induce antigen-specific Th1 and Th17 immune responses, thus, predisposing the host to colitis following exposure to an otherwise innocuous inflammatory insult.

Provocateurs and triggers: induction of antigen-specific responses to the colonic resident microbiota and susceptibility to colitis