ArticleCell host & microbe2025
Targeted inhibition of pathobiont virulence factor mitigates alcohol-associated liver disease.
Article in Cell host & microbe, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed.
- Article
- Escherichia coli expressing the kpsM gene exacerbates drug-induced liver injury through up-regulating α1,2-fucosyltransferase and disturbing the host taurine metabolism-from animal models and clinical studies.Journal of advanced research · 2026Article
- Covert hepatic encephalopathy as a multi-organ syndrome: the gut-liver-muscle-brain axis, diagnosis, treatment, and multidisciplinary care.Journal of gastroenterology · 2026Review
- Gut Microbiota and Ageing: A Critical Crosstalk in Alcohol-Related Liver Disease.Microorganisms · 2026Review
- BRD4 modulates antimicrobial defense via non-canonical NRF2 activation in macrophages to confer protection against sepsis.PLoS pathogens · 2026Article
- Gut microbiome and bile acid metabolism in liver disease: Mechanisms, clinical implications, and therapeutic opportunities.Pharmacological reviews · 2026Review
- Gut microbiome in alcohol-associated liver disease: interactions and therapeutic strategies.Frontiers in pharmacology · 2026Review
- Review
- Review
- Metagenome Analysis Reveals Changes in Gut Microbial Antibiotic Resistance Genes and Virulence Factors in Reintroduced Giant Pandas.Microorganisms · 2025Article
- Metabolic dysfunction and alcohol-associated liver disease (MetALD).eGastroenterology · 2025Review
Corrections and comments
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Authors and funding
32 authors.
Funding
Abstract
Alcohol-associated liver disease poses a global health burden with high mortality. Imbalances in the gut microbiota are important for disease progression. Using metagenomic sequencing of fecal samples from a multicenter, international cohort of patients with alcohol-associated hepatitis, we found that the presence of virulence factor KpsM, encoded in the genome of Escherichia coli (E. coli), correlated with patient mortality. Functional studies using gnotobiotic mouse models and genetic manipulation of bacteria demonstrated that kpsM-positive E. coli exacerbate ethanol-induced liver disease. The kpsM gene mediates the translocation of capsular polysaccharides to the cell surface. This enables kpsM-positive E. coli to evade phagocytosis by the scavenger receptor Marco on Kupffer cells in the liver, leading to bacterial spread. Importantly, inhibiting kpsM-dependent capsules with the small molecule 2-(4-phenylphenyl)benzo[g]quinoline-4-carboxylic acid (C7) attenuated ethanol-induced liver disease in mice. We show that precision targeting of the virulence factor KpsM is a promising approach to improve outcomes of patients with alcohol-associated hepatitis.
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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 OpenQuestion graph.