ArticleJournal of immunology (Baltimore, Md. : 1950)2014
PPAR-γ/IL-10 axis inhibits MyD88 expression and ameliorates murine polymicrobial sepsis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
51 citing papers in PubMed, 78 citations in OpenAlex.
- PPARγ-Dependent Pioglitazone Treatment Suppresses Neuroinflammation and Improves Cognition in Sepsis-Associated Encephalopathy in Mice.CNS neuroscience & therapeutics · 2026Article
- Diagnostic potential of circular RNAs in carotid atherosclerotic plaque vulnerability.Non-coding RNA research · 2026Article
- Myeloid-derived interleukin-10 induced by thrombospondin-1 mediates host defense and regulates inflammation during acute bacterial lung infection.Infection and immunity · 2026Article
- Selenium and Selenoproteins in Neutrophil Functions.Biological trace element research · 2026Review
- GATA2 mutation is associated with immune dysfunction and increased Mycobacterium haemophilum susceptibility in immunocompromised individuals.JCI insight · 2025Article
- Nuclear receptors in health and disease: signaling pathways, biological functions and pharmaceutical interventions.Signal transduction and targeted therapy · 2025Review
- Evaluation of the Effect of an α-Adrenergic Blocker, a PPAR-γ Receptor Agonist, and a Glycemic Regulator on Chronic Kidney Disease in Diabetic Rats.International journal of molecular sciences · 2024Article
- Bovine lactoferrin inhibits inflammatory response and apoptosis in lipopolysaccharide-induced acute lung injury by targeting the PPAR-γ pathway.Molecular biology reports · 2024Article
- Botanical formulation HX110B ameliorates PPE-induced emphysema in mice via regulation of PPAR/RXR signaling pathway.PloS one · 2024Article
- Review
- The role of peroxisome proliferator-activated receptors in the modulation of hyperinflammation induced by SARS-CoV-2 infection: A perspective for COVID-19 therapy.Frontiers in immunology · 2023Review
- Studies on the contribution of PPAR Gamma to tuberculosis physiopathology.Frontiers in cellular and infection microbiology · 2023Article
- Review
- Pioglitazone Modifies Kupffer Cell Function and Protects againstInternational journal of molecular sciences · 2022Article
- Physiological Convergence and Antagonism Between GR and PPARγ in Inflammation and Metabolism.Advances in experimental medicine and biology · 2022Review
- The Role of PPAR-γ in Allergic Disease.Current allergy and asthma reports · 2021Review
- Macrophage-Derived MicroRNA-21 Drives Overwhelming Glycolytic and Inflammatory Response during Sepsis via Repression of the PGEJournal of immunology (Baltimore, Md. : 1950) · 2021Article
- LMWF5A suppresses cytokine release by modulating select inflammatory transcription factor activity in stimulated PBMC.Journal of translational medicine · 2020Article
- TICAM2-related pathway mediates neutrophil exhaustion.Scientific reports · 2020Article
- Oxidative Stress in Ischemic Heart Disease.Oxidative medicine and cellular longevity · 2020Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
Polymicrobial sepsis induces organ failure and is accompanied by overwhelming inflammatory response and impairment of microbial killing. Peroxisome proliferator-activated receptor (PPAR)-γ is a nuclear receptor with pleiotropic effects on lipid metabolism, inflammation, and cell proliferation. The insulin-sensitizing drugs thiazolidinediones (TZDs) are specific PPAR-γ agonists. TZDs exert anti-inflammatory actions in different disease models, including polymicrobial sepsis. The TZD pioglitazone, which has been approved by the U.S. Food and Drug Administration, improves sepsis outcome; however, the molecular programs that mediate its effect have not been determined. In a murine model of sepsis, we now show that pioglitazone treatment improves microbial clearance and enhances neutrophil recruitment to the site of infection. We also observed reduced proinflammatory cytokine production and high IL-10 levels in pioglitazone-treated mice. These effects were associated with a decrease in STAT-1-dependent expression of MyD88 in vivo and in vitro. IL-10R blockage abolished PPAR-γ-mediated inhibition of MyD88 expression. These data demonstrate that the primary mechanism by which pioglitazone protects against polymicrobial sepsis is through the impairment of MyD88 responses. This appears to represent a novel regulatory program. In this regard, pioglitazone provides advantages as a therapeutic tool, because it improves different aspects of host defense during sepsis, ultimately enhancing survival.
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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.