ArticleNature communications2024
Biosynthetic enzyme analysis identifies a protective role for TLR4-acting gut microbial sulfonolipids in inflammatory bowel disease.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Bacterial lipid structural diversity mediates commensalism and pathogenesis.Nature reviews. Microbiology · 2026Review
- Gut-liver metabolic and enterohormonal remodeling drives progression from metabolic dysfunction-associated steatotic liver disease to steatohepatitis.Metabolism: clinical and experimental · 2026Article
- Lipopolysaccharide hydrolysis-targeting nano-chimeras detoxify endotoxin through specific adsorption and efficient degradation.Nature communications · 2026Article
- Synthesis and Evaluation of Sulfobacin A and Analogues for Their Roles in Immunological Recognition.ACS medicinal chemistry letters · 2026Article
- Article
- Multi-Omic Insights Into Mediterranean Diet-Associated Microbiota.Molecular nutrition & food research · 2026Article
- Reduction in microbiota-derived short-chain fatty acids contributes to the pathogenesis of pulmonary arterial hypertension.Respiratory research · 2026Article
- Genetics-mediated regulation of intestinal gene expression on microbiome contributes to human disease heritability.Molecular systems biology · 2026Article
- Metagenomic analysis of human feces reveals gut microbiome role in colorectal cancer.Frontiers in cellular and infection microbiology · 2026Article
- Ornithine lipids fromGut microbes · 2025Article
- Sulfur-Containing Microbial Natural Products and Their Role in Communal Interactions.Journal of natural products · 2025Review
- Human gut commensalGut microbes · 2025Article
- Emerging strategies to enhance microbial natural product-based drug discovery.Current opinion in biotechnology · 2025Review
- From gut to liver: Exploring the relationship between inflammatory bowel disease and metabolic dysfunction-associated steatotic liver disease.World journal of hepatology · 2025Review
- Metabolomic, Lipidomic, and Enterohormone Changes in the Progression from MASLD to MASH.bioRxiv : the preprint server for biology · 2025Article
- An Updated and Comprehensive Review Exploring the Gut-Brain Axis in Neurodegenerative Disorders and Neurotraumas: Implications for Therapeutic Strategies.Brain sciences · 2025Review
- Six Interferon-Stimulated Genes as Biomarkers of M1 Macrophage Polarization in Psoriasis.Journal of inflammation research · 2025Article
- Deciphering the immunocellular regulatory network in inflammatory bowel disease: from susceptibility genes to cellular effectors and toward precision therapies.Frontiers in immunology · 2025Review
- Oral Administration of Crocus sativus Tepals Extract Restores High-Fat Diet-Induced Gut Dysbiosis and Modulates Intestinal Inflammation and Hepatic Lipid Metabolism.BioFactors (Oxford, England)Article
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15 authors.
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Abstract
The trillions of microorganisms inhabiting the human gut are intricately linked to human health. While specific microbes have been associated with diseases, microbial abundance alone cannot reveal the molecular mechanisms involved. One such important mechanism is the biosynthesis of functional metabolites. Here, we develop a biosynthetic enzyme-guided disease correlation approach to uncover microbial functional metabolites linked to disease. Applying this approach, we negatively correlate the expression of gut microbial sulfonolipid (SoL) biosynthetic enzymes to inflammatory bowel disease (IBD). Targeted chemoinformatics and metabolomics then confirm that SoL abundance is significantly decreased in IBD patient data and samples. In a mouse model of IBD, we further validate that SoL abundance is decreased while inflammation is increased in diseased mice. We show that SoLs consistently contribute to the immunoregulatory activity of different SoL-producing human microbes. We further reveal that sulfobacins A and B, representative SoLs, act on Toll-like receptor 4 (TLR4) and block lipopolysaccharide (LPS) binding, suppressing both LPS-induced inflammation and macrophage M1 polarization. Together, these results suggest that SoLs mediate a protective effect against IBD through TLR4 signaling and showcase a widely applicable biosynthetic enzyme-guided disease correlation approach to directly link the biosynthesis of gut microbial functional metabolites to human health.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.