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The Citrobacter rodentium Mouse Model: Studying Pathogen and Host Contributions to Infectious Colitis
Published on: February 19, 2013
An antibiotic depleted microbiome drives severe Campylobacter jejuni-mediated Type 1/17 colitis, Type 2 autoimmunity
Phillip T Brooks1, Julia A Bell2, Christopher E Bejcek3
1Comparative Enteric Diseases Laboratory, Michigan State University, East Lansing, MI, USA; Comparative Medicine Integrative Biology Graduate Program, Michigan State University, East Lansing, MI, USA; College of Veterinary Medicine, Michigan State University, East Lansing, MI, USA; Institute for Integrative Toxicology, Michigan State University, East Lansing, MI, USA.
Abstract:
The peripheral neuropathy Guillain-Barré Syndrome can follow Campylobacter jejuni infection when outer core lipooligosaccharides induce production of neurotoxic anti-ganglioside antibodies. We hypothesized that gut microbiota depletion with an antibiotic would increase C. jejuni colonization, severity of gastroenteritis, and GBS. Microbiota depletion increased C. jejuni colonization, invasion, and colitis with Type 1/17 T cells in gut lamina propria. It also stimulated Type 1/17 anti-C. jejuni and -antiganglioside-antibodies, Type 2 anti-C. jejuni and -antiganglioside antibodies, and neurologic phenotypes. Results indicate that both C. jejuni strain and gut microbiota affect development of inflammation and GBS and suggest that probiotics following C. jejuni infection may ameliorate inflammation and autoimmune disease.
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