ArticleFrontiers in pharmacology2016
Rifaximin Improves Clostridium difficile Toxin A-Induced Toxicity in Caco-2 Cells by the PXR-Dependent TLR4/MyD88/NF-κB Pathway.
Article in Frontiers in pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- Trial
- Targeting PPARγ-NF-κB: (+)-catechin reversesFuture microbiology · 2026Article
- Exploring the Therapeutic Role of Pregnane X Receptor Activation in Acute Kidney Injury: Mechanisms and Clinical Implications.Current molecular medicine · 2026Review
- Indole Propionic Acid Regulates Gut Immunity: Mechanisms of Metabolite-Driven Immunomodulation and Barrier Integrity.Journal of microbiology and biotechnology · 2025Review
- Role of peripheral inflammation in minimal hepatic encephalopathy.Metabolic brain disease · 2024Review
- Article
- Review
- Microbial Metabolites as Ligands to Xenobiotic Receptors: Chemical Mimicry as Potential Drugs of the Future.Drug metabolism and disposition: the biological fate of chemicals · 2023Review
- Dual therapy with zinc acetate and rifaximin prevents from ethanol-induced liver fibrosis by maintaining intestinal barrier integrity.World journal of gastroenterology · 2021Article
- Microbiota-Immune Interactions in Ulcerative Colitis and Colitis Associated Cancer and Emerging Microbiota-Based Therapies.International journal of molecular sciences · 2021Review
- Prevention of Cirrhosis Complications: Looking for Potential Disease Modifying Agents.Journal of clinical medicine · 2021Review
- The Use of Rifaximin in Patients With Cirrhosis.Hepatology (Baltimore, Md.) · 2021Review
- Rifaximin Modulates the Gut Microbiota to Prevent Hepatic Encephalopathy in Liver Cirrhosis Without Impacting the Resistome.Frontiers in cellular and infection microbiology · 2021Article
- Potential role of drug metabolizing enzymes in chemotherapy-induced gastrointestinal toxicity and hepatotoxicity.Expert opinion on drug metabolism & toxicology · 2020Review
- Increased Endotoxin Activity Is Associated with the Risk of Developing Acute-on-Chronic Liver Failure.Journal of clinical medicine · 2020Article
- Rifaximin Alleviates Endotoxemia with Decreased Serum Levels of Soluble CD163 and Mannose Receptor and Partial Modification of Gut Microbiota in Cirrhotic Patients.Antibiotics (Basel, Switzerland) · 2020Article
- The xenobiotic sensing pregnane X receptor regulates tissue damage and inflammation triggered by C difficile toxins.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Mechanism of action and therapeutic benefit of rifaximin in patients with irritable bowel syndrome: a narrative review.Therapeutic advances in gastroenterology · 2020Review
- Pathogenesis of Hepatic Encephalopathy in Chronic Liver Disease.Journal of clinical and experimental hepatology · 2018Review
- Article
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11 authors.
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Abstract
backgroundClostridium difficile infections (CDIs) caused by Clostridium difficile toxin A (TcdA) lead to severe ulceration, inflammation and bleeding of the colon, and are difficult to treat.
aimThe study aimed to evaluate the effect of rifaximin on TcdA-induced apoptosis in intestinal epithelial cells and investigate the role of PXR in its mechanism of action.
methodsCaco-2 cells were incubated with TcdA and treated with rifaximin (0.1-10 μM) with or without ketoconazole (10 μM). The transepithelial electrical resistance (TEER) and viability of the treated cells was determined. Also, the expression of zona occludens-1 (ZO-1), toll-like receptor 4 (TLR4), Bcl-2-associated X protein (Bax), transforming growth factor-β-activated kinase-1 (TAK1), myeloid differentiation factor 88 (MyD88), and nuclear factor-kappaB (NF-κB) was determined.
resultsRifaximin treatment (0.1, 1.0, and 10 μM) caused a significant and concentration-dependent increase in the TEER of Caco-2 cells (360, 480, and 680% vs. TcdA treatment) 24 h after the treatment and improved their viability (61, 79, and 105%). Treatment also concentration-dependently decreased the expression of Bax protein (-29, -65, and -77%) and increased the expression of ZO-1 (25, 54, and 87%) and occludin (71, 114, and 262%) versus TcdA treatment. The expression of TLR4 (-33, -50, and -75%), MyD88 (-29, -60, and -81%) and TAK1 (-37, -63, and -79%) were also reduced with rifaximin versus TcdA treatment. Ketoconazole treatment inhibited these effects.
conclusionRifaximin improved TcdA-induced toxicity in Caco-2 cells by the PXR-dependent TLR4/MyD88/NF-κB pathway mechanism, and may be useful in the treatment of CDIs.
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