Abstract

Benign prostatic hyperplasia (BPH) is a highly prevalent age-associated condition characterized by progressive 
enlargement of the prostate and lower urinary tract symptoms that significantly impair quality of life. 
Traditionally regarded as a hormonally driven disorder, BPH is now increasingly recognized as a chronic 
inflammatory disease in which immune dysregulation plays a central pathogenic role. Immune profiling studies of 
prostatic tissue, peripheral blood, and expressed prostatic secretions have consistently demonstrated persistent 
infiltration of innate and adaptive immune cells, accompanied by sustained cytokine and chemokine production. 
This chronic inflammatory milieu promotes epithelial and stromal proliferation, extracellular matrix remodeling, 
smooth muscle hypercontractility, and fibrotic changes that collectively drive prostate enlargement and functional 
obstruction. Emerging evidence also highlights the interaction between immune activation, oxidative stress, 
cellular senescence, aging, and metabolic dysfunction as critical amplifiers of inflammatory signaling in BPH. 
Importantly, interindividual variability in immune signatures correlates with prostate volume, symptom severity, 
and therapeutic responsiveness, underscoring the clinical relevance of immune heterogeneity. This section 
synthesizes current knowledge on immune cell composition, inflammatory mediators, and mechanistic pathways 
linking chronic inflammation to prostatic remodeling. Understanding immune profiling in BPH provides a 
framework for redefining disease pathogenesis and supports the development of targeted immunomodulatory 
strategies as adjuncts or alternatives to conventional therapies.