The Role of Inflammation and Immune Dysregulation in the Pathogenesis of BPH

Benign prostatic hyperplasia (BPH) is a prevalent non-cancerous enlargement of the prostate that affects a significant proportion of aging men, often resulting in bothersome lower urinary tract symptoms (LUTS). While traditionally linked to hormonal imbalances, particularly dihydrotestosterone (DHT), emerging evidence has increasingly highlighted the critical role of chronic inflammation and immune dysregulation in BPH pathogenesis. Inflammatory infiltrates comprising immune cells such as macrophages, lymphocytes, and neutrophils are frequently observed in the prostates of men with BPH. This inflammatory response promotes cellular proliferation, disrupts apoptosis, and induces fibrosis, leading to prostate enlargement. Factors such as infections, autoimmune reactions, and oxidative stress contribute to this chronic inflammatory environment, which is further exacerbated by systemic inflammation associated with aging and metabolic disturbances. This review explores the mechanisms by which chronic inflammation drives BPH progression, including cytokine-mediated cell proliferation and growth factor-induced fibrosis, as well as the imbalance between pro-apoptotic and anti-apoptotic signaling in prostate tissues. Furthermore, it delves into the potential of immune-targeted therapies as a novel approach to treating BPH, focusing on cytokine inhibitors, immune modulation, and anti-inflammatory agents. These therapies, which address the underlying inflammatory processes in BPH, offer promise in not only alleviating symptoms but also in slowing disease progression. By understanding the role of inflammation and immune dysregulation in BPH, novel therapeutic strategies may emerge, potentially revolutionizing the management of this common condition. Keywords: Benign prostatic hyperplasia (BPH), Chronic inflammation, Immune dysregulation, Prostate enlargement, Immune-targeted therapies