ArticleInternational journal of molecular sciences2021
Pro-Inflammatory Effects of Indoxyl Sulfate in Mice: Impairment of Intestinal Homeostasis and Immune Response.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 57 citations in OpenAlex.
- Indoxyl sulfate exacerbates chronic inflammation and susceptibility to severe infection via modulating T-cell CD73/adenosine signaling in chronic kidney disease.Renal failure · 2026Article
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- Microbiota-driven tryptophan metabolism and AhR triggered intestinal stem cell differentiation: mechanisms of huangqin decoction in ulcerative colitis repair.Chinese medicine · 2026Article
- Microbiota-gut-kidney axis in health and renal disease.International journal of biological sciences · 2026Review
- Host-microbial co-metabolites: from biogenesis to immunomodulation and implications for health and disease.Frontiers in immunology · 2026Review
- Plumericin Modulates the AhR-NFκB-Nrf2 Signaling Network to Counteract Indoxyl Sulfate-Induced Intestinal Epithelial Cells Impairment.International journal of molecular sciences · 2025Article
- Targeting Inflammatory Imbalance in Chronic Kidney Disease: Focus on Anti-Inflammatory and Resolution Mediators.International journal of molecular sciences · 2025Review
- Plasma and Visceral Organ Kynurenine Metabolites Correlate in the Multiple Sclerosis Cuprizone Animal Model.International journal of molecular sciences · 2025Article
- LncRNA NEAT1 protects uremic toxin-induced intestinal epithelial barrier injury by regulating miR-122-5p/Occludin axis.PloS one · 2025Article
- Bidirectional Interaction Between Chronic Kidney Disease andJournal of immunology research · 2025Article
- Association between serum total indoxyl sulfate, intraperitoneal inflammation, and peritoneal dialysis technique failure: a 3-year prospective cohort study.BMC nephrology · 2024Article
- Gut microbiota regulates oxidative stress and inflammation: a double-edged sword in renal fibrosis.Cellular and molecular life sciences : CMLS · 2024Review
- Redefining Roles: A Paradigm Shift in Tryptophan-Kynurenine Metabolism for Innovative Clinical Applications.International journal of molecular sciences · 2024Review
- Qingfei Zhisou oral liquid alleviates fever-induced inflammation by regulating arachidonic acid and lysophospholipids metabolism and inhibiting hypothalamus transient receptor potential ion channels expression.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2024Article
- Does the Composition of Gut Microbiota Affect Chronic Kidney Disease? Molecular Mechanisms Contributed to Decreasing Glomerular Filtration Rate.International journal of molecular sciences · 2024Review
- Article
- Review
- Resveratrol Mitigates Uremic Toxin-Induced Intestinal Barrier Dysfunction in Chronic Kidney Disease by Promoting Mitophagy and Inhibiting Apoptosis Pathways.International journal of medical sciences · 2024Article
- Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
The intestines are recognized as the main source of chronic inflammation in chronic kidney disease (CKD) and, among other cells, macrophages are involved in modulating this process as well as in the impaired immune response which also occurs in CKD patients. In this study, we evaluated the effect of Indoxyl Sulfate (IS), a protein bound uremic toxin poorly eliminated by hemodialysis, on inflammatory, oxidative stress and pro-apoptotic parameters, at the intestinal level in mice, on intestinal epithelial cells (IEC-6) and on primary murine peritoneal macrophages. C57BL/6J mice were treated with IS (800 mg/kg i.p.) for 3 or 6 h and histopathological analysis showed that IS induced intestinal inflammation and increased cyclooxygenase-2 (COX-2), nitrotyrosine and Bax expression in intestinal tissue. In IEC-6 cells, IS (125-1000 µM) increased tumor necrosis factor-α levels, COX-2 and inducible nitric oxide synthase expression and nitrotyrosine formation. Moreover, IS increased pro-oxidant, pro-inflammatory and pro-apoptotic parameters in peritoneal macrophages from IS-treated mice. Also, the serum concentration of IS and pro-inflammatory levels of cytokines resulted increased in IS-treated mice. Our results indicate that IS significantly contributes to affect intestinal homeostasis, immune response, and to induce a systemic pro-inflammatory state thus highlighting its potential role as therapeutic target in CKD patients.
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Registered trials
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