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- Academic Editor
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†These authors contributed equally.
Background: The cause of ulcerative colitis (UC) is not yet fully
understood. Previous research has pointed towards a potential role for mutations
in nucleotide-binding oligomerization domain-containing protein 2 (NOD2) in promoting the onset and progression of inflammatory bowel disease
(IBD) by altering the microbiota of the gut. However, the relationship between
toll-like receptor 4 (TLR4) and gut microbiota in IBD is not well understood. To
shed light on this, the interaction between TLR4 and gut microbiota was studied
using a mouse model of IBD. Methods: To examine the function of TLR4
signaling in intestinal injury repair, researchers developed Dextran Sulfate
Sodium Salt (DSS)-induced colitis and injury models in both wild-type (WT) mice
and TLR4 knockout (TLR4-KO) mice. To assess changes in the gut microbiota, 16S
rRNA sequencing was conducted on fecal samples from both the TLR4-KO and WT
enteritis mouse models. Results: The data obtained depicted a protective
function of TLR4 against DSS-induced colitis. The gut microbiota composition was
found to vary considerably between the WT and TLR4-KO mice groups as indicated by