The gut-prostate axis in benign prostatic hyperplasia: systematic review of microbial dysbiosis and pathogenic mechanisms.

Significant differences in beta-diversity were observed in the gut microbiota of BPH patients compared to controls.

• The systematic review included a total of 10 preclinical studies and 6 clinical studies.
• Studies covered 413 patients with BPH and 338 controls in total.
• Five different types of BPH mouse models were also included across the preclinical studies.
• Databases searched included PubMed, MEDLINE, and Web of Science from establishment through October 7, 2025.

An increased Firmicutes/Bacteroidetes (F/B) ratio was identified as a marker of the pathological condition of BPH.

• A significant increase in the F/B ratio was regarded as a marker of the pathological condition in BPH.
• This finding was consistent across the included clinical and preclinical studies.
• The increased F/B ratio is described as a characteristic feature of gut microbiota dysbiosis in BPH.

Changes in the abundances of Prevotella, Ruminococcus, and Lactobacillus may play a key role in the pathogenesis of BPH.

• Specifically, a decreased abundance of Lactobacillus was identified as a potentially important factor.
• Alterations in Prevotella and Ruminococcus abundances were also highlighted as relevant to BPH pathogenesis.
• These specific microbial changes were identified across clinical and/or preclinical studies included in the review.

Imbalance of interleukin-6 (IL-6) and interleukin-18 (IL-18) may be related to the pathogenesis of BPH.

• Both IL-6 and IL-18 levels were implicated in BPH pathogenesis through the gut-prostate axis.
• These inflammatory indicators are proposed as potential diagnostic means and therapeutic targets for BPH.
• The inflammatory imbalance was identified as one of several pathogenic mechanisms linking gut microbiota dysbiosis to BPH.

Changes in the levels of intestinal tight junction protein-1 and claudin-1 may be related to the pathogenesis of BPH.

• Alterations in intestinal tight junction protein-1 and claudin-1 were identified as markers of intestinal barrier dysfunction relevant to BPH.
• These markers of intestinal barrier dysfunction are proposed as potential diagnostic means and therapeutic targets.
• Intestinal barrier dysfunction is presented as a pathogenic mechanism connecting gut dysbiosis to BPH development.

Gut microbiota dysbiosis and associated metabolites, inflammatory indicators, and intestinal barrier dysfunction markers may become effective diagnostic means and potential therapeutic targets for BPH.

• The review synthesized evidence from both clinical studies (413 BPH patients, 338 controls) and preclinical studies (5 BPH mouse models).
• Specific factors identified as potential targets include the F/B ratio, Lactobacillus abundance, IL-6, IL-18, tight junction protein-1, and claudin-1.
• The authors conclude that the specific characteristics of gut microbiota in BPH patients have not yet been fully clarified, indicating a need for further research.
• The gut-prostate axis is proposed as a framework for understanding BPH pathogenesis.