Vaginal trichomoniasis, caused by Trichomonas vaginalis, is the most common sexually transmitted disease. However, despite its high prevalence, the pathogenesis of T. vaginalis infection has not been clearly characterized although neutrophil infiltration is considered to be primarily responsible for the cytologic changes associated with this infection. We investigated that trichomonads in the vagina sometime after an acute infection secrete proteins like excretory-secretory product that have a chemotactic effect on neutrophils, and that these neutrophils are further stimulated by T. vaginalis to produce chemokines like IL-8 and GRO-α, which further promote neutrophil recruitment and chemotaxis. Thus, neutrophil accumulation is believed to maintain or aggravate inflammation. However, enhanced neutrophil apoptosis induced by live T. vaginalis could contribute to resolution of inflammation via anti-inflammatory cytokine produced by human macrophage phagocytosed of apoptotic neutrophils. Macrophages may constitute an important component of host defense against T. vaginalis infection, and may be involved in inflammation via production of proinflammatory cytokines and nitric oxide. In the host, T. vaginalis uses a capping phenomenon and cleave host immunoglobulins with proteinases as the evasion methods from host immune responses. Recently, we developed a highly sensitive and specific diagnostic polymerase chain reaction (PCR) technique, and found that the method enables the detection of T. vaginalis at concentrations as low as 1 cell per PCR mixture.