# Prostatitis-Related Male Infertility: From Inflammation and Dysbiosis to Sperm DNA Damage

## TL;DR

This review explores how prostatitis causes male infertility through inflammation, microbial imbalances, and sperm DNA damage, and suggests a new diagnostic and treatment approach.

## Contribution

The paper introduces a diagnostic framework for prostatitis-related infertility integrating inflammation, oxidative stress, and microbiome markers.

## Key findings

- Leukocytospermia and elevated interleukin-8 are linked to impaired sperm motility and increased DNA fragmentation.
- Persistent infection or dysbiosis contributes to immune activation and oxidative stress in prostatitis.
- Seminal cytokines and microbes may influence female reproductive tract biology, though data is limited.

## Abstract

Prostatitis includes infectious and noninfectious inflammatory phenotypes that can impair male reproductive potential and may influence couple-level reproduction via seminal inflammatory and microbial exposure. This review summarizes mechanisms linking prostatic inflammation and dysbiosis to semen dysfunction and sperm DNA damage and proposes an infertility-oriented diagnostic and management framework. This is a narrative review of clinical and translational evidence addressing semen inflammation, oxidative stress, sperm DNA fragmentation (SDF), microbiome signatures, and reproductive outcomes in prostatitis (National Institutes of Health (NIH) categories I-IV). Across prostatitis phenotypes, leukocytospermia and elevated seminal cytokines (especially interleukin-8) are associated with impaired motility, altered viscosity and liquefaction, oxidative stress, and higher SDF. Persistent infection or dysbiosis may sustain immune activation and redox injury, while ductal remodeling and pain-related sexual dysfunction can further reduce natural conception. Seminal cytokines and microbes may affect female reproductive tract biology, although clinical outcome data remain limited. Prostatitis-related infertility requires evaluation beyond routine semen analysis. A biomarker-guided workup integrating inflammatory markers, oxidative stress testing, targeted microbiology (culture plus nucleic acid amplification tests when indicated), SDF testing in selected men, and imaging when obstruction is suspected can identify treatable drivers and guide timing and selection of assisted reproduction strategies. Future studies should standardize fertility endpoints and validate biomarker-guided and microbiome-directed interventions.