Proneness of TLR5 deficient mice to develop colitis is microbiota dependent

Vishal Singh, Beng San Yeoh, Frederic Carvalho, Andrew T. Gewirtz, Matam Vijay-Kumar

Research output: Contribution to journalArticle

17 Scopus citations


Alterations in the gut microbiota have been implicated to play a role in potentiating inflammatory bowel diseases in both humans and mice. Mice lacking the flagellin receptor, toll-like receptor 5 (TLR5), are prone to develop spontaneous gut inflammation, but are significantly protected when treated with antibiotics or maintained in germ-free conditions. However, given that the incidence of spontaneous inflammation in TLR5KO mice is quite variable in conventional conditions (typically ∼10% show clear colitis), this result is far from definitive and does not rule out that TLR5KO mice might be prone to develop inflammation even in the absence of a microbiota. Herein, we demonstrate that neutralization of IL10 signaling induces colitis in 100% of TLR5KO mice which provide a more rigorous approach to evaluate the role of microbiota in gut inflammation. Mice treated with antibiotics or maintained in germ-free condition are substantially protected against IL-10R neutralization-induced colitis, underscoring that gut inflammation in TLR5KO mice is dependent upon the presence of a gut microbiota.

Original languageEnglish (US)
Pages (from-to)279-283
Number of pages5
JournalGut microbes
Issue number4
Publication statusPublished - Jan 1 2015


All Science Journal Classification (ASJC) codes

  • Microbiology
  • Gastroenterology
  • Microbiology (medical)
  • Infectious Diseases

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