ArticlePrecision clinical medicine2024
Suppression of MyD88 disturbs gut microbiota and activates the NLR pathway and hence fails to ameliorate DSS-induced colitis.
Article in Precision clinical medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 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
- Regulation of Inducible Nitric Oxide Synthase (NOS2) Expression in Healthy and Inflamed Bowel: A Narrative Review.International journal of molecular sciences · 2026Review
- Dysfunction of mitochondria in intestinal epithelial cells: a key player in the pathogenesis of inflammatory bowel diseases.Gastroenterology report · 2026Review
- Review
- Abnormal intestinal microbial colonization in prenatally stressed offspring is related to lung and intestinal cytokine expression.Frontiers in microbiology · 2026Article
- Mechanistic Interplay of Gut Microbiota and Blood-Brain Barrier Integrity in Neurodegenerative Diseases.Molecular neurobiology · 2025Review
- The Role of Microbiota in the Pathogenesis of Bullous Pemphigoid and Pemphigus Vulgaris: Evidence, Controversies, and Perspectives.International journal of molecular sciences · 2025Review
- Genes, guts, and microbes: decoding host-driven microbial regulation using intestine-specific conditional knockouts.Frontiers in immunology · 2025Review
- The microbiota: a crucial mediator in gut homeostasis and colonization resistance.Frontiers in microbiology · 2024Review
- Astaxanthin Alleviates Inflammatory Response in Neonatal Necrotizing Enterocolitis Rats by Regulating NOD2/TLR4 Pathway.Gastroenterology research and practice · 2023Article
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Myeloid differentiation factor 88 (MyD88) is the core adaptor for Toll-like receptors defending against microbial invasion and initiating a downstream immune response during microbiota-host interaction. However, the role of MyD88 in the pathogenesis of inflammatory bowel disease is controversial. This study aims to investigate the impact of MyD88 on intestinal inflammation and the underlying mechanism. Methods: MyD88 knockout (MyD88 Results: In an acute DSS-colitis model, the severity of colitis was not alleviated in MyD88 Conclusion: Our study suggests that the suppression of MyD88 might be associated with unfavorable changes in the composition of gut microbiota, leading to NLR-mediated immune activation and intestinal inflammation.
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