Proneness of TLR5 deficient mice to develop colitis is microbiota dependent.
Gut Microbes, 2015/7/04;6(4):279-83.
Singh V[1], Yeoh BS, Carvalho F, Gewirtz AT, Vijay-Kumar M
Affiliations
PMID: 26067589DOI: 10.1080/19490976.2015.1060390
Impact factor: 9.434
Abstract
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.
Keywords: Abx; Germ-free mice; Gut bacteria; Interleukin-10; Intestinal inflammation; Toll-like receptor; antibiotics; GF; germ-free; IL-10; interleukin 10; MPO; myeloperoxidase.
MeSH terms
Animals; Anti-Bacterial Agents; Colitis; Gastrointestinal Microbiome; Germ-Free Life; Interleukin-10; Mice; Mice, Knockout; Receptors, Interleukin-10; Toll-Like Receptor 5
More resources
Full text:
Europe PubMed Central; PubMed Central
EndNote: Download