ArticleMilitary Medical Research2025
High-salt-driven gut microbiota dysfunction aggravates prostatitis by promoting AHR/SGK1/FOXO1 axis-mediated Th17 cell differentiation.
Article in Military Medical Research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Synthetic microbial communities: emerging live biotherapeutics for targeted gut microbiome modulation.Gut microbes · 2026Review
- The gut-prostate axis in benign prostatic diseases: Mechanistic pathways and therapeutic implications.iScience · 2026Review
- T cell-derived CCL5 drives macrophage immunometabolic remodeling in chronic prostatitis via the CCR5-ERK-PKM2/HIF-1α axis.Redox biology · 2026Article
- Development and evaluation of a novel experimental autoimmune prostatitis model induced by a prostate-specific antigen mixture in rats.Biochemistry and biophysics reports · 2026Article
- Review
- CXCR4 inhibition alleviates prostatic inflammation and pelvic pain via suppressing Th17 cell differentiation and oxidative stress in EAP mice.International journal of biological sciences · 2026Article
- Immune remodeling in chronic prostatitis: from microenvironment imbalance to targeted therapy.Frontiers in molecular biosciences · 2026Article
- High-salt diet promotes atopic dermatitis by partially enhancing intestinal SGK1/ENaC signaling and destroying gutFrontiers in cellular and infection microbiology · 2026Article
- The multifaceted impact of a high-salt environment on the immune system and its contribution to salt-sensitive hypertension.Biochemistry and biophysics reports · 2025Review
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Authors and funding
13 authors.
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Abstract
backgroundChronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a frequently encountered disorder characterized by voiding symptoms and pelvic or perineal pain. Proinflammatory T helper 17 (Th17) cells are essential for triggering the development of CP/CPPS. High-salt diet (HSD) consumption has been found to cause an accumulation of sodium chloride in peripheral organs, inducing autoimmune responses via the Th17 cell axis. It is currently unknown whether HSD affects the etiology and course of CP/CPPS.
methodsPatients diagnosed with CP/CPPS were evaluated with the National Institutes of Health Chronic Prostatitis Symptom Index scoring system, and the correlation between the symptoms of CP/CPPS with HSD was analyzed. The experimental autoimmune prostatitis (EAP) mouse was established and the mice were fed either a normal-salt diet (NSD) or HSD for 6 weeks to investigate the impact of HSD on CP/CPPS. Then, 16S ribosomal RNA sequencing and untargeted metabolomics were introduced to detect the differences in the gut microflora composition and metabolite profiles between NSD-fed and HSD-fed mice, followed by fecal microbiota transplantation, 5-hydroxyindole acetic acid (5-HIAA) supplementation, aryl hydrocarbon receptor (AHR) inhibition, and in vitro Th17 differentiation experiments, which were performed to explore the mechanisms underlying HSD-aggravated CP/CPPS. Finally, chromatin immunoprecipitation assay and quantitative polymerase chain reaction were conducted to validate whether AHR can serve as a transcription factor by interacting with the serum and glucocorticoid-regulated kinase 1 (Sgk1) promoter in CD4
resultsIncreased salt consumption had a positive correlation with symptom scores of CP/CPPS patients, which was validated by feeding EAP mice with HSD, and HSD worsened the prostate inflammation and tactile allodynia in EAP mice through promoting the differentiation of CD4
conclusionOur findings indicated that high salt intake represented a risk factor for the development of CP/CPPS as it promoted the differentiation of CD4
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