Benign prostatic hyperplasia (BPH) is one of the most common urologic diseases, and its incidence continues to increase. Although its pathogenesis remains incompletely understood, accumulating evidence suggests that chronic inflammation is involved in the initiation and progression of BPH. Accordingly, BPH is increasingly regarded as an immune-inflammatory disease, and targeted anti-inflammatory therapy has emerged as a promising research direction. This review summarizes the role of chronic inflammation in BPH, focusing on immune cells, inflammatory mediators, nuclear factor kappa-B (NF-κB), the NOD-like receptor protein 3 (NLRP3) inflammasome, the T helper cell 17 (Th17)/Interleukin-17 (IL-17) axis, and other related signaling pathways in the prostate. It also discusses the interactions between inflammation, metabolic syndrome (MetS), and the gut microbiota, and reviews the current status of anti-inflammatory therapy for BPH, with the aim of providing a theoretical basis for targeted anti-inflammatory treatment.