ArticleScientific reports2024
NLRP3-mediated IL-1β in regulating the imbalance between Th17 and Treg in experimental autoimmune prostatitis.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Targeting the brain-gut-prostate axis in chronic prostatitis: mechanisms and therapeutics.Frontiers in endocrinology · 2025Pooled it
- T cell-derived CCL5 drives macrophage immunometabolic remodeling in chronic prostatitis via the CCR5-ERK-PKM2/HIF-1α axis.Redox biology · 2026Article
- Current Perspectives on the Inflammatory Bowel Disease Pathogenesis of Microbiota and the Gut-Brain Axis, and Emerging Therapeutics.Biomedicines · 2026Review
- NLRP3 inflammasome regulates Th17/Treg cell balance in experimental autoimmune myocarditis.Biochemistry and biophysics reports · 2026Article
- UHPLC-Q-Orbitrap-HRMS-Based Multilayer Mapping of the Pharmacodynamic Substance Basis and Mechanistic Landscape of Maizibizi Wan in Chronic Nonbacterial Prostatitis Therapy.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Orchestrating the gut microbiota-mitochondrial-immune axis in gynecological diseases: mechanisms and dual-targeting therapeutic strategies.Frontiers in reproductive health · 2026Review
- Immune remodeling in chronic prostatitis: from microenvironment imbalance to targeted therapy.Frontiers in molecular biosciences · 2026Article
- Antibiotic-induced gut microbiota dysbiosis and bile acid metabolism: implications for intestinal health, immune regulation, and disease susceptibility.Frontiers in microbiology · 2026Review
- Spatiotemporal regulation of acute wound healing by the NLRP3 inflammasome: dual roles in macrophage-fibroblast chemotaxis and phenotype during wound repair.Burns & trauma · 2026Article
- Antibiotic cocktail-induced changes in gut microbiota drive alteration of bile acid metabolism to restrain Th17 differentiation through the FXR-NLRP3 axis.Gut microbes · 2025Article
- Naringin mitigates experimental autoimmune prostatitis by modulating oxidative stress and the NLRP3 inflammasome via the PPAR-γ/NF-κB pathway.Scientific reports · 2025Article
- An anti-complement homogeneous polysaccharide fromActa pharmaceutica Sinica. B · 2025Article
- How Cells Die in Psoriasis?International journal of molecular sciences · 2025Review
- Immunometabolism in the Aging Heart.Journal of the American Heart Association · 2025Review
- Gut microbiota dysbiosis in diabetic nephropathy: mechanisms and therapeutic targeting via the gut-kidney axis.Frontiers in endocrinology · 2025Review
- Immune Cells Phenotypes and Causal Relationship with Acne Vulgaris: Insights from Mendelian Randomization.Clinical, cosmetic and investigational dermatology · 2025Article
- Article
- Regulatory Mechanism and Drug Therapy of NLRP3 Inflammasome in Recurrent Pregnancy Loss: Research Status and Prospect.Journal of inflammation research · 2025Review
- Gut microbiota in hypothyroidism: pathogenic mechanisms and opportunities for precision microbiome interventions.Frontiers in microbiology · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a urinary disorder that affects youthful to middle-aged men most frequently. It has been revealed that Th17/Treg imbalance is a crucial factor in the pathophysiological mechanisms behind this disease. However, this imbalance's mechanisms are unknown. In the experimental autoimmune prostatitis (EAP) mouse model, the NLRP3 inflammasome was turned on, IL-1β levels went up. Moreover, there exists a discernible positive association between the upsurge in IL-1β and the perturbation of Th17/Treg equilibrium. Additionally, we have revealed that IL-1β plays a vital role in promoting the differentiation of Naïve CD4+ T cells into the Th17 cells and enhances the conversion of Treg cells into Th17 cells. Further studies revealed that IL-1β promotes STAT3 phosphorylation, which is what causes Treg cells to become Th17 cells. All data strongly suggest that the NLRP3 inflammatory influence Th17 cell development and the conversion of Treg cells into Th17 cells through IL-1β, disrupting the Th17/Treg balance and exacerbating EAP inflammation. In this article, we provide new theories for the pathogenesis of CP/CPPS and propose new prevention and therapy methods.
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Registered trials
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