Alcohol intake exacerbates experimental autoimmune prostatitis through activating PI3K/AKT/mTOR pathway-mediated Th1...

Area of Science:

• Urology
• Immunology
• Pharmacology

Background:

• Epidemiological studies link alcohol consumption to chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS).
• Mechanisms underlying alcohol's impact on CP/CPPS remain unclear.
• This study investigates alcohol's effects on CP/CPPS using an animal model and human data.

Purpose of the Study:

• To determine how alcohol consumption affects CP/CPPS.
• To elucidate the molecular mechanisms involved in alcohol-induced CP/CPPS exacerbation.
• To identify potential therapeutic targets for CP/CPPS.

Main Methods:

• Established the experimental autoimmune prostatitis (EAP) mouse model.
• Administered alcohol during EAP induction and assessed inflammation.
• Utilized proteomic analysis, flow cytometry, and Western blotting to investigate mechanisms.
• Included patients with chronic alcohol consumption for clinical correlation.

Main Results:

• Alcohol consumption exacerbated EAP severity in mice and patients.
• Abnormal Th1 differentiation and PI3K/AKT/mTOR pathway activation were identified.
• Alcohol activated the PI3K/AKT/mTOR pathway, increasing Th1 cell differentiation.
• PI3K inhibition (LY294002) reduced Th1 differentiation and alleviated EAP inflammation.

Conclusions:

• Alcohol intake promotes Th1 cell differentiation and exacerbates EAP by activating the PI3K/AKT/mTOR pathway.
• The PI3K/AKT/mTOR pathway is a key mediator of alcohol's detrimental effects in CP/CPPS.
• Inhibiting the PI3K/AKT/mTOR pathway offers a potential therapeutic strategy for CP/CPPS.