Human trichomonosis, infection with Trichomonas vaginalis, is the most common non-viral sexually transmitted disease in the world. The host-parasite interaction and pathophysiological processes of trichomonosis remain incompletely understood. This review focuses on the advancements reached in the area of the pathogenesis of T. vaginalis, especially in the role of the cysteine proteinases. It highlights various approaches made in this field and lists a group of trichomonad cysteine proteinases involved in diverse processes such as invasion of the mucous layer, cytoadherence, cytotoxicity, cytoskeleton disruption of red blood cells, hemolysis, and evasion of the host immune response. A better understanding of the biological roles of cysteine proteinases in the pathogenesis of this parasite could be used in the identification of new chemotherapeutic targets. An additional advantage could be the development of a vaccine in order to reduce transmission of T. vaginalis.

Trichomonas vaginalis infects the epithelium of the genital tract. The mechanism by which it invades the tissue leading to the disease is not thoroughly understood. However, results of several studies seem to agree that parasite adhesion to epithelium cells is the initial step leading to infection in women. T. vaginalis is associated with high levels of proteolytic activity. The role of some of these proteinases in the development of infection has been demonstrated. The current study establishes the role of a 62 kDa excretion-secretion proteinase in parasite cytoadherence. Monoclonal antibodies (MAbs) against this enzyme were tested for their ability to inhibit this process. Three stable hybrid producers of IgG(1)class MAbs (4D8, 1A8, 3C11) against the 62 kDa proteinase were obtained. Two of them (4D8 and 1A8) showed parasite recognition by immunofluorescence. Parasite cytoadherence to a monolayer of HeLa cells was inhibited by the 4D8, 1A8 and 3C11 antibodies. MAb 4D8 administered 24 h before a challenge with T. vaginalis by the intraperitoneal route was able to protect the majority of mice. Nitric oxide levels in the serum of animals inoculated with MAb 4D8 and challenged with the parasite were significantly different from those recorded in mice treated with an unrelated MAb. These studies show that an appropriate antibody against 62 kDa proteinase can help the host resist a challenge by the intraperitoneal route with T. vaginalis.

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The aim of this study was to analyze the presence of 62 kDa proteinase and anti-62 kDa proteinase antibody in clinical samples of symptomatic and asymptomatic infected women. Proteinase was detected in all the swabs vaginal of infected women. Significantly, amounts of antigen (mean optical density (OD) values) were detected in swabs vaginal of symptomatic as compared to asymptomatic women. This protein was not detected in the group of patients with Trichomonas vaginalis-culture-negative results and in the groups of samples infected with other agents. Antibody to 62 kDa was detected in the swabs vaginal the only 66.6% of the symptomatic and 55.5% of the asymptomatic infected women. Antibody to 62 kDa was also detected in 7/30 of the swabs vaginal from uninfected women. No significant difference was observed in mean OD values of vaginal swabs of T. vaginalis-infected symptomatic as compared to asymptomatic women. The presence of proteinase in 100% of T. vaginalis-infected women suggested that 62 kDa proteinase could be a virulence factor.

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