Role of interleukins, IGF and stem cells in BPH

Abstract

The condition known as benign prostatic hyperplasia may be defined as a benign enlargement of the prostate gland resulting from a proliferation of both benign epithelial and stromal elements. It might also be defined clinically as a constellation of lower urinary tract symptoms (LUTSs) in aging men. The purpose of this review is to consider the ways in which inflammatory cytokines belonging to the interleukin family, members of the IFG family, and stem cells may contribute to the development and progression of BPH-LUTS. This might occur in three mechanisms: One, interleukin signaling, IFG signaling and stem cells may contribute to reactivation of developmental growth mechanisms in the adult prostate leading to tissue growth. Two, given that epidemiologic studies indicate an increased incidence of BPH-LUTS in association with obesity and diabetes, IFG signaling may provide the mechanistic basis for the effect of diabetes and obesity on prostate growth. Three, expression of interleukins in association with inflammation in the prostate may induce sensitization of afferent fibers innervating the prostate and result in increased sensitivity to pain and noxious sensations in the prostate and bladder and heightened sensitivity to bladder filling.

Fig. 1

Proposed mechanism for the interaction of inflammatory signalling, systemic insulin response, and the sensitization of afferent nerve fibers in BPH/LUTS.