Inflammatory response to Trichomonas vaginalis in the pathogenesis of prostatitis and benign prostatic hyperplasia

Abstract

<i>Trichomonas vaginalis</i> is a flagellated protozoan that causes trichomoniasis, a common nonviral sexually transmitted infection. <i>T. vaginalis</i> infection is asymptomatic in most infected men but can lead to chronic infection. The inflammatory response to chronic <i>T. vaginalis</i> infection may contribute to prostatic diseases, such as prostatitis and benign prostatic hyperplasia (BPH); however, studies on the relationship between <i>T. vaginalis</i> infection and prostate diseases are scarce. In this review, we discuss evidence from our studies on the involvement of <i>T. vaginalis</i> in the pathogenesis of prostate diseases, such as prostatitis and BPH. Studies of prostatitis have demonstrated that the attachment of <i>T. vaginalis</i> trophozoite to prostate epithelial cells (PECs) induces inflammatory cytokine production and inflammatory cell migration, leading to prostatitis. <i>T. vaginalis</i> also causes pathological changes, such as inflammatory cell infiltration, acinar changes, interstitial fibrosis, and mast cell infiltration, in prostate tissues of infected rats. Thus, <i>T. vaginalis</i> is considered an infectious agent that triggers prostatitis. Meanwhile, studies of prostatic hyperplasia revealed that mast cells activated by <i>T. vaginalis</i>-infected prostate cells secreted inflammatory mediators, such as β-hexosaminidase and tryptase, which promoted proliferation of prostate stromal cell (PSC). Moreover, interleukin-6 produced by proliferating PSCs induced the multiplication of BPH-1 epithelial cells as a result of stromal–epithelial interaction, suggesting that the proliferation of <i>T. vaginalis</i>-infected prostate cells can be induced through crosstalk with mast cells. These collective findings suggest that <i>T. vaginalis</i> contributes to the progression of prostatitis and prostatic hyperplasia by creating an inflammatory microenvironment involving PECs and PSCs.