ArticleThe Prostate2026
Epigenetic Regulation of Immune Dysfunction in Chronic Prostatitis/Chronic Pelvic Pain Syndrome.
Article in The Prostate, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Immune remodeling in chronic prostatitis: from microenvironment imbalance to targeted therapy.Frontiers in molecular biosciences · 2026Article
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9 authors.
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Abstract
backgroundChronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a prevalent and debilitating condition with unclear etiology. Increasing evidence implicates immune dysregulation, yet the molecular mechanisms underlying impaired immune regulation remain poorly defined. This study investigated the role of altered immune responses within PBMC populations and DNA methylation in CP/CPPS pathogenesis.
methodsPost-prostatic massage urine samples designated as Voided Bladder 3 (VB3) urine from CP/CPPS patients and healthy controls were analyzed for CD4
resultsVB3 samples from CP/CPPS patients demonstrated elevated CD4-associated transcripts and increased expression of immune-related transcription factors including RORγT. DNA methylation analysis identified differences in methylation across immune-regulatory loci including IL10, FOXP3, CD274, ITGAL, and TNF-α. PBMCs from patients exhibited diminished IL10 secretion in response to LPS, which was restored by AZA treatment. In the EAP model, recombinant IL10 administration failed to attenuate pelvic allodynia, whereas AZA significantly reduced pain sensitivity.
conclusionsCP/CPPS is associated with epigenetic alterations in immune regulatory genes that may influence inflammatory responses. Pharmacologic inhibition of DNA methylation enhanced IL10 responses in vitro and reduced pain behaviors in vivo, supporting demethylation therapy as a potential strategy for treating chronic prostatic inflammation and pelvic pain.
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