P. gingivalis in oral-prostate axis exacerbates benign prostatic hyperplasia via IL-6/IL-6R pathway

Area of Science:

• Oral Microbiology
• Urology
• Pathogenesis Research

Background:

• Benign prostatic hyperplasia (BPH) is a prevalent condition in aging men.
• Periodontitis is increasingly linked to BPH risk, but the underlying mechanisms are not fully understood.
• This study investigates the role of Porphyromonas gingivalis (P. gingivalis), a key periodontal pathogen, in BPH development.

Purpose of the Study:

• To explore the role and mechanism of Porphyromonas gingivalis in the development of benign prostatic hyperplasia (BPH).
• To investigate the association between P. gingivalis and BPH in patients and animal models.

Main Methods:

• Collected subgingival plaque and prostatic fluid from BPH patients with periodontitis for 16S rDNA sequencing.
• Established rat models for periodontitis, BPH, and a combined condition.
• Injected P. gingivalis and its lipopolysaccharide (P.g-LPS) into rat prostates and used P.g-LPS to create prostate cell infection models.

Main Results:

• P. gingivalis was frequently detected in the prostatic fluid of BPH patients with periodontitis.
• P. gingivalis infection and P.g-LPS significantly induced prostate epithelial and stromal hyperplasia and collagen fibrosis.
• P. gingivalis promoted prostate cell proliferation, inhibited apoptosis, and upregulated IL-6, IL-6Rα, and gp130 via the Akt pathway, driving BPH.

Conclusions:

• Porphyromonas gingivalis is abundant in the prostatic fluid of patients with concurrent BPH and periodontitis.
• P. gingivalis infection contributes to BPH development.
• The progression of BPH may be influenced by P. gingivalis-induced inflammation and activation of the Akt signaling pathway.