{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,12]],"date-time":"2026-02-12T11:15:55Z","timestamp":1770894955872,"version":"3.50.1"},"reference-count":52,"publisher":"MDPI AG","issue":"2","license":[{"start":{"date-parts":[[2026,2,4]],"date-time":"2026-02-04T00:00:00Z","timestamp":1770163200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Pathogens"],"abstract":"<jats:p>Metabolic Dysfunction-Associated Steato-Hepatitis (MASH) is a multiple-hit disease. Endotoxins, ethanol, and other metabolites of certain gut microbiota can reach the liver and accelerate inflammation and disease progression. Targeting ethanol-producing colonic bacteria with rifaximin could affect the progress of MASH. In the present study, thirty mice were assigned to three groups (n = 10 mice per group). Mice received either a normal diet, a Western diet, or a Western diet with oral rifaximin. After 12 weeks, liver function, serum levels of TNF-\u03b1, interleukin (IL)-1\u03b2, IL-6, and lipopolysaccharides (LPS) were measured. Liver specimens were assessed for pathological changes, lipid deposition, and fibrosis. Expression of p53, GFAP, CD68, and TLR-4 in the liver was also assessed. Faecal samples were evaluated for ethanol contents. Lactobacillus acidophilus, in addition to ethanol-producing Klebsiella pneumoniae and Escherichia coli, were isolated, quantified, and tested for sensitivity to rifaximin. Rifaximin was able to ameliorate Western diet-induced biochemical changes and elevated TNF-\u03b1, IL-1\u03b2, IL-6, and LPS levels. Changes in liver histology, fibrosis, and lipid content were attenuated. Expressions of p53, GFAP, CD68, and TLR-4 in the liver were all reduced. The Western diet-induced increases in faecal ethanol or ethanol-producing bacteria were not corrected by rifaximin. After 12 weeks, isolated bacteria from the rifaximin group were rifaximin-resistant. Our findings imply that the protective impact of rifaximin in the MASH model is unlikely to be mediated by alteration of ethanol-producing colonic bacteria because of acquired rifaximin resistance. Rifaximin-induced reduction in endotoxemia and inflammation in the liver appears to be a more relevant explanation.<\/jats:p>","DOI":"10.3390\/pathogens15020170","type":"journal-article","created":{"date-parts":[[2026,2,5]],"date-time":"2026-02-05T10:35:37Z","timestamp":1770287737000},"page":"170","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Rifaximin Protects Against Inflammation and Fibrosis in MASH: Any Role for Ethanol-Producing Bacteria?"],"prefix":"10.3390","volume":"15","author":[{"given":"Mohamed","family":"Abouelkheir","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Therapeutics, College of Medicine, Jouf University, Sakaka City 72388, Saudi Arabia"},{"name":"Department of Pharmacology, College of Medicine, Mansoura University, Mansoura City 35516, Egypt"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0121-3211","authenticated-orcid":false,"given":"Dalia A.","family":"Shabaan","sequence":"additional","affiliation":[{"name":"Department of Medical Histology and Cell Biology, Faculty of Medicine, Mansoura University, Mansoura City 35516, Egypt"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5766-4495","authenticated-orcid":false,"given":"Ahmed E.","family":"Taha","sequence":"additional","affiliation":[{"name":"Microbiology and Immunology Unit, Department of Pathology, College of Medicine, Jouf University, Sakaka City 72388, Saudi Arabia"},{"name":"Department of Medical Microbiology and Immunology, Faculty of Medicine, Mansoura University, Mansoura City 35516, Egypt"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2026,2,4]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"150","DOI":"10.1111\/apt.17846","article-title":"Implications of the New Nomenclature of Steatotic Liver Disease and Definition of Metabolic Dysfunction-associated Steatotic Liver Disease","volume":"59","author":"Loomba","year":"2024","journal-title":"Aliment. 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