The role of microbiota in the chronic prostatitis/chronic pelvis pain syndrome: a review

Abstract

Chronic prostatitis/Chronic pelvis pain syndrome (CP/CPPS), a kind of frequent urinary condition among adult males, has caused a lot of inconvenience to patients in life, whose pathogenesis is unclear. Current evidence suggests that it is most likely to be an autoimmune disease. Symbiotic microbes, a highly diverse biological community that harbors trillions of microbes in each region of the human body, have gradually made people realize their important role in immune regulation, material metabolism, and health maintenance. In recent years, increasing studies have shown a connection between microbiota and CP/CPPS. In view of this, we performed this review to summarize the literature pertaining to microbiota and its association with the pathophysiological mechanism of CP/CPPS. In addition, we gleaned the latest progress in the therapeutic strategy of CP/CPPS that related to microbiota regulation in order to offer new perspectives on the management of CP/CPPS.

Keywords: CP/CPPS; microbiota; pathogenesis; treatment; treatment microbiota.

FIGURE 1

Various microbiota of different regions and chronic prostatitis/chronic pelvis pain syndrome (CP/CPPS). Microbiota present in the gut, oral cavity, urinary system, and semen have proven to correlate with etiopathogenesis as well as the treatment of CP/CPPS.

FIGURE 2

The gut-prostate axis: immune mechanism. SCFAs produced by gut microbiota decomposing dietary fibers in food possess the ability to regulate the proliferation and differentiation of immune cells via the corresponding G protein-coupled receptor pathway. Gut microbiota-derived SCFAs propionate can promote the differentiation of initial T cells to Treg cells and inhibit their differentiation to Th17 cells via the GPR43-HDAC-6 axis, with the former secreting anti-inflammatory cytokines and the latter secreting pro-inflammatory cytokines. Furthermore, gut microbiota up-regulate Th17 cell ratios and their responses through microbial-associated cholesterol metabolism pathways, exacerbating the inflammatory response. The relative balance of Th17/Treg is critical in the inflammatory environment of the prostate. This immune mechanism by which the gut microbiota and its metabolites drive host immune regulation has further deepened researchers’ understanding of the gut-prostate axis. (SCFAs, short chain fat acids; GPR, G protein-coupled receptor; HDAC, histone deacetylase).

FIGURE 3

The possible mechanisms of oral microbiota-induced chronic prostatitis/chronic pelvis pain syndrome (CP/CPPS). Oral pathogens may reach the prostate via hematogenous spread, thereby directly injuring prostate tissue. In addition to this, oral pathogens may mediate the production and dissemination of pro-inflammatory factors, such as IL-1β, IL-2, IL-6, IL-8, TNF-α, and CRP that indirectly trigger CP/CPPS onset. This hypothesis of an indirect pathogenic pathway provides an argument for systemic immune disorders to lead to CP/CPPS. (IL, interleukin; TNF-α, tumor necrosis factor-α; CRP, C-reactive protein).