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Effect of depletion of intestinal TLR4 on gene expression of small intestine

ABSTRACT: To investigate the effect of altered intestinal TLR4 expression on acute pancreatitis, we established intestines‐specific TLR4 KO mice in which TLR4 gene has been knocked down by CRISPR-Cas9 We then performed gene expression profiling analysis using data obtained from RNA-seq of gut of wide type mice（n=3） and TLR4ΔIEC mice（n=3）

ORGANISM(S): Mus musculus

PROVIDER: GSE200780 | GEO | 2023/04/26

REPOSITORIES: GEO

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The protective role of TLR4 in intestinal epithelial cells through the regulation of the gut microbiota in DSS-induced colitis in mice

Project description:Abstract. Background: The cause of ulcerative colitis (UC) is not yet fully understood. Previous research has pointed towards a potential role for mutations in 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 β-diversity analysis and operational taxonomic units (OTUs) cluster. Statistical analysis of microbial multivariate variables depicted an elevated abundance of Escherichia coli/Shigella, Gammaproteobacteria, Tenerlcutes, Deferribacteres, Enterobacteria, Rikenellaceae, and Proteobacteria in the gut microbiota of TLR4-KO mice, whereas there was a considerable reduction in Bacteroidetes at five different levels of the phylogenetic hierarchy including phylum, class, order, family, and genus in comparison with the WT control. Conclusion: TLR4 may protect intestinal epithelial cells from damage in response to DSS-induced injury by controlling the microbiota in the gut.

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Gene expression accompanying the promotion of hepatocellular carcinoma by intestinal microbiota and Tlr4 in mice.

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Project description:The effect of Tlr4P712H mutation (rendering TLR4 non-functional), or gut-sterilization by antbiotics, on the induction of tumorgenesis by CCl4 and diethylnitrosamine (DEN) was characterized. Affymetrix Mouse 430 2.0 gene expression measurements were used to characterize the transcriptomic basis of the effects of the above treatments and genotypes on tumorgenesis. Gene expression of mouse livers of A. Normal liver from WT C3H/HeOuJ mice, B. HCC from WT C3H/HeOuJ mice treated with CCl4 and DEN, C.HCC from TLR4-mutant C3H/HeJ mice (Tlr4P712H) treated with CCl4 and DEN and D.HCC from WT C3H/HeOuJ mice treated with antibiotics (a combination of ampicillin (1 g/l), neomycin [1 g/l], metronidazole[1 g/l] and vancomycin [500 mg/l] in drinking water) and CCl4 and DEN were characterized.

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Project description:This study shows that the TLR4/MyD88 pathway in intestinal mesenchymal cells promotes intestinal carcinogenesis in the APCmin mouse model.

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