ArticleExperimental & molecular medicine2018
Administration of antibiotics contributes to cholestasis in pediatric patients with intestinal failure via the alteration of FXR signaling.
Article in Experimental & molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 45 papers, 2 of them syntheses that pooled it.
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Who cites it
45 citing papers in PubMed, 2 syntheses or guidelines pooled it, 76 citations in OpenAlex.
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- The role of FGF19-FGFR4 signaling pathway in liver health and disease: Guardian or destroyer.Genes & diseases · 2026Review
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- Antibiotic-induced gut microbiota dysbiosis and bile acid metabolism: implications for intestinal health, immune regulation, and disease susceptibility.Frontiers in microbiology · 2026Review
- Unveiling Butyrate as a Parkinson's Disease Therapy.Neuroscience bulletin · 2026Review
- Fecal Microbiome and Bile Acid Profiles Differ in Preterm Infants with Parenteral Nutrition-associated Cholestasis.Journal of clinical and translational hepatology · 2025Article
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- Signaling pathways and targeted therapy for pulmonary hypertension.Signal transduction and targeted therapy · 2025Review
- Mitochondrial Dysfunction-Molecular Mechanisms and Potential Treatment approaches of Hepatocellular Carcinoma.Molecular and cellular biochemistry · 2025Review
- Emerging role and clinical applications of circular RNAs in human diseases.Functional & integrative genomics · 2025Review
- High-altitude pulmonary hypertension: a comprehensive review of mechanisms and management.Clinical and experimental medicine · 2025Review
- Niclosamide modulates phenotypic switch and inflammatory responses in human pulmonary arterial smooth muscle cells.Molecular and cellular biochemistry · 2025Article
- Clostridium Scindens Protects Against Vancomycin-Induced Cholestasis and Liver Fibrosis by Activating Intestinal FXR-FGF15/19 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Dietary purslane modulates gut microbiota and fecal metabolites in aging rats.Frontiers in microbiology · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The link between antibiotic treatment and IF-associated liver disease (IFALD) is unclear. Here, we study the effect of antibiotic treatment on bile acid (BA) metabolism and investigate the involved mechanisms. The results showed that pediatric IF patients with cholestasis had a significantly lower abundance of BA-biotransforming bacteria than patients without cholestasis. In addition, the BA composition was altered in the serum, feces, and liver of pediatric IF patients with cholestasis, as reflected by the increased proportion of primary BAs. In the ileum, farnesoid X receptor (FXR) expression was reduced in patients with cholestasis. Correspondingly, the serum FGF19 levels decreased significantly in patients with cholestasis. In the liver, the expression of the rate-limiting enzyme in bile salt synthesis, cytochrome P450 7a1 (CYP7A1), increased noticeably in IF patients with cholestasis. In mice, we showed that oral antibiotics (gentamicin, GM or vancomycin, VCM) reduced colonic microbial diversity, with a decrease in both Gram-negative bacteria (GM affected Eubacterium and Bacteroides) and Gram-positive bacteria (VCM affected Clostridium, Bifidobacterium and Lactobacillus). Concomitantly, treatment with GM or VCM decreased secondary BAs in the colonic contents, with a simultaneous increase in primary BAs in plasma. Moreover, the changes in the colonic BA profile especially that of tauro-beta-muricholic acid (TβMCA), were predominantly associated with the inhibition of the FXR and further altered BA synthesis and transport. In conclusion, the administration of antibiotics significantly decreased the intestinal microbiota diversity and subsequently altered the BA composition. The alterations in BA composition contributed to cholestasis in IF patients by regulating FXR signaling.
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