ArticleCell reports2025
MyD88-mediated signaling in intestinal fibroblasts regulates macrophage antimicrobial defense and prevents dysbiosis in the gut.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Lactobacillus brevis cell-free supernatant attenuates inflammation-associated gene expression and differentially modulates host defense-associated genes in DSS-stimulated HT-29 cells.Molecular biology reports · 2026Article
- From inflammation to fibrosis and cancer: the emerging role of AIEC-derived metabolites in intestinal disease progression.Experimental & molecular medicine · 2026Review
- Distribution of gut microbiota and prognostic value in elderly patients with coronary atherosclerosis: a preliminary culture-based study.BMC cardiovascular disorders · 2026Article
- Research hotspots and frontiers in the tumor microenvironment of gastric cancer: a bibliometric review from 2005 to 2024.Translational cancer research · 2025Article
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Authors and funding
13 authors.
Funding
Abstract
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 dextran sulfate sodium (DSS)-induced colitis. These pathological changes were associated with the accumulation of Arginase 1
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