ArticleMicrobiome2024
Desulfovibrio vulgaris interacts with novel gut epithelial immune receptor LRRC19 and exacerbates colitis.
Article in Microbiome, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 56 citations in OpenAlex.
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- Integrated omics reveal the effects of vitamin D deficiency on gut microbiota and plasma metabolism in experimental autoimmune uveitis.Journal of neuroinflammation · 2026Article
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- Taoling Yuyang Decoction alleviates DSS-induced ulcerative colitis in mice by regulating gut microbiota -metabolite axis and restore intestinal barrier function.Frontiers in microbiology · 2026Article
- Decoding the power of the microbiome in human health.Frontiers in cellular and infection microbiology · 2026Review
- Integrated Multi-Omics, Machine Learning, and Single-Cell Analysis Provide Insights into Potential Multi-Target Candidate Mechanisms of Combined MAGL11 and Icaritin in Alleviating Imidazole Propionate-Driven Metabolic Intestinal Injury.Drug design, development and therapy · 2026Article
- Dietary L-arginine supplementation exerts preventive effects on colitis through modulation of the gut microbiota.Frontiers in nutrition · 2026Article
- Characteristics of gut microbiota and metabolites in rats with ketamine-induced cystitis.Scientific reports · 2025Article
- Whole microbiota transplantation restores gut homeostasis throughout the gastrointestinal tract.iMeta · 2025Article
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Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe overgrowth of Desulfovibrio, an inflammation promoting flagellated bacteria, has been found in ulcerative colitis (UC) patients. However, the molecular mechanism in promoting colitis remains unestablished.
methodsThe relative abundance Desulfovibrio vulgaris (D. vulgaris) in stool samples of UC patients was detected. Mice were treated with dextran sulfate sodium to induce colitis with or without administration of D. vulgaris or D. vulgaris flagellin (DVF), and the severity of colitis and the leucine-rich repeat containing 19 (LRRC19) signaling were assessed. The interaction between DVF and LRRC19 was identified by surface plasmon resonance and intestinal organoid culture. Lrrc19
resultsD. vulgaris was enriched in fecal samples of UC patients and was correlated with the disease severity. D. vulgaris or DVF treatment significantly exacerbated colitis in germ-free mice and conventional mice. Mechanistically, DVF could interact with LRRC19 (rather than TLR5) in colitis mice and organoids, and then induce the production of pro-inflammatory cytokines. Lrrc19 knockdown blunted the severity of colitis. Furthermore, typhaneoside, a blockade of binding interfaces, blocked DVF-LRRC19 interaction and dramatically ameliorated DVF-induced colitis.
conclusionsD. vulgaris could promote colitis through DVF-LRRC19 interaction. Targeting DVF-LRRC19 interaction might be a new therapeutic strategy for UC therapy. Video Abstract.
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