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

## TL;DR

This study reviews how gut microbiota imbalances may contribute to benign prostatic hyperplasia, highlighting potential diagnostic and therapeutic targets.

## Contribution

The paper systematically reviews preclinical and clinical evidence linking gut microbiota dysbiosis to BPH pathogenesis.

## Key findings

- Gut microbiota in BPH patients show altered β-diversity and increased Firmicutes/Bacteroidetes ratio.
- Changes in Prevotella, Ruminococcus, and Lactobacillus abundances are linked to BPH development.
- Inflammatory markers like IL-6 and IL-18, along with intestinal barrier dysfunction, are associated with BPH.

## Abstract

New evidence shows that gut microbiota dysbiosis may play a crucial role in the development process of benign prostatic hyperplasia (BPH). However, at present, the specific characteristics of the gut microbiota in patients with BPH have not been fully clarified.

The PubMed, MEDLINE and Web of Science databases were systematically searched to find the clinical and preclinical studies related to the relationship between BPH and gut microbiota from the establishment of the databases to October 7, 2025. And the studies reporting on gut microbiota and BPH were analyzed.

A total of 10 preclinical studies and 6 clinical studies were included. These studies covered 413 patients with BPH, 338 controls, and 5 different types of BPH mouse models in total. Compared with the control group, there were significant differences in β-diversity in the BPH group. A significant increase in the Firmicutes/Bacteroidetes (F/B) ratio was regarded as a marker of the pathological condition. Specifically, changes in the abundances of Prevotella, Ruminococcus, and Lactobacillus may play a key role in the pathogenesis of the occurrence and development of BPH. The imbalance of interleukin-6 (IL-6) and interleukin-18 (IL-18), as well as changes in the levels of intestinal tight junction protein-1 and claudin-1, may also be related to the pathogenesis of BPH.

Changes in the abundances of specific gut microbiota and their metabolites, such as an increased F/B ratio and a decreased abundance of Lactobacillus, as well as the levels of inflammatory indicators and markers of intestinal barrier dysfunction, may play a crucial role in the pathogenesis of BPH. These factors may become effective diagnostic means and potential therapeutic targets for BPH.

The online version contains supplementary material available at 10.1186/s12894-025-02003-2.