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MyD88-mediated signaling in intestinal fibroblasts regulates macrophage antimicrobial defense and prevents dysbiosis in the gut IV

ABSTRACT: MyD88-mediated signaling in intestinal fibroblasts regulates macrophage antimicrobial defense and prevents dysbiosis in the gut IV

PROVIDER: PRJNA1232159 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32577044_1.fastq.gz	Fastqsanger.gz
	SRR32577044_2.fastq.gz	Fastqsanger.gz
	SRR32577045_1.fastq.gz	Fastqsanger.gz
	SRR32577045_2.fastq.gz	Fastqsanger.gz
	SRR32577046_1.fastq.gz	Fastqsanger.gz

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MyD88-mediated signaling in intestinal fibroblasts regulates macrophage antimicrobial defense and prevents dysbiosis in the gut IV

Project description:Fibroblasts that reside in the gut mucosa are among the key regulators of innate immune cells, but their role in the regulation of the defense functions of macrophages remains unknown. MyD88 is suggested to shape fibroblast responses in the intestinal microenvironment. We found that mice lacking MyD88 in fibroblasts showed a decrease in the colonic antimicrobial defense, developing dysbiosis and aggravated DSS-induced colitis. These pathological changes were associated with accumulation of Arginase 1+ macrophages with low antimicrobial defense capability. Mechanistically, production of IL-6 and CCL2 downstream of MyD88 was critically involved in fibroblast-mediated support of macrophage antimicrobial function, and IL-6/CCL2 neutralization resulted in the generation of macrophages with decreased production of antimicrobial peptide cathelicidin and impaired bacterial clearance. Collectively, these findings revealed a critical role of fibroblast-intrinsic MyD88 signaling in regulating macrophage antimicrobial defense under colonic homeostasis, and its disruption results in dysbiosis, predisposing host to the development of intestinal inflammation.

2025-03-05 | GSE291184 | GEO

MyD88-mediated signaling in intestinal fibroblasts regulates macrophage antimicrobial defense and prevents dysbiosis in the gut I

2025-03-05 | GSE291179 | GEO

MyD88-mediated signaling in intestinal fibroblasts regulates macrophage antimicrobial defense and prevents dysbiosis in the gut III

2025-03-05 | GSE291182 | GEO

MyD88-mediated signaling in intestinal fibroblasts regulates macrophage antimicrobial defense and prevents dysbiosis in the gut II

2025-03-05 | GSE291180 | GEO

MyD88-mediated signaling in intestinal fibroblasts regulates macrophage antimicrobial defense and prevents dysbiosis in the gut III

Project description:MyD88-mediated signaling in intestinal fibroblasts regulates macrophage antimicrobial defense and prevents dysbiosis in the gut III

| PRJNA1232155 | ENA

MyD88-mediated signaling in intestinal fibroblasts regulates macrophage antimicrobial defense and prevents dysbiosis in the gut II

Project description:MyD88-mediated signaling in intestinal fibroblasts regulates macrophage antimicrobial defense and prevents dysbiosis in the gut II

| PRJNA1232145 | ENA

MyD88-mediated signaling in intestinal fibroblasts regulates macrophage antimicrobial defense and prevents dysbiosis in the gut I

Project description:MyD88-mediated signaling in intestinal fibroblasts regulates macrophage antimicrobial defense and prevents dysbiosis in the gut I

| PRJNA1232146 | ENA

Autophagy regulator DRAM1 functions downstream of MYD88 in defense against tuberculosis

Project description:Autophagy regulator DRAM1 functions downstream of MYD88 in defense against tuberculosis

| PRJNA213243 | ENA

MyD88-mediated signaling prevents development of adenocarcinomas of the colon via interleukin-18

Project description:Inflammation has pleiotropic effects on carcinogenesis and tumor progression. Signaling through the adaptor protein MyD88 promotes carcinogenesis in several chemically induced cancer models. Interestingly, we observed a protective role for MyD88 in the development of AOM/DSS colitis-associated cancer. The inability of Myd88-/- mice to heal ulcers generated upon injury creates an inflammatory environment that increases the frequency of mutations and results in a dramatic increase in adenoma formation and cancer progression. Susceptibility to colitis development and enhanced polyp formation were also observed in Il18-/- mice upon AOM/DSS treatment, suggesting that the phenotype of MyD88 knockouts is in part due to their inability to signal through the IL-18 receptor. This study revealed a previously unknown level of complexity surrounding MyD88 activities downstream of different receptors that differentially impact tissue homeostasis and carcinogenesis. The Myd88 knockout mice were backcrossed to obtain at least 98% congenicity to B6NCr background. As control groups, wild type mice of identical background were used. Ten biological repeats were performed for the treated wild type and Myd88 samples. Six biological repeats were performed for the untreated wild type and Myd88 samples.

2010-07-30 | E-GEOD-19793 | biostudies-arrayexpress

Autophagy regulator DRAM1 functions downstream of MYD88 in defense against tuberculosis (array)

Project description:MyD88 is an adaptor protein in Toll-like receptor and interleukin 1 receptor mediated signaling pathways that plays an essential role in activation of immune responses following pathogen recognition. We investigate that role in the zebrafish embryo model by using a zebrafish mutant line that contains a premature stop condon in the gene encoding MyD88, leading to a truncated protein that lacks domains important for its normal function. We infected these MyD88 mutants and wildtype individuals with S Mycobacterium marinum to compare the resulting immune response by transcriptome profiling on total RNA isolated from single embryos. Autophagy regulator dram1 was identified as one of the MyD88-dependent genes.

2014-06-01 | GSE49187 | GEO

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