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Trichomoniasis, a common cause of vaginitis, is the most common sexually transmitted infection in humans, worldwide. It is caused by infection with the single-celled protozoan parasite, Trichomonas vaginalis, which disrupts normal vaginal flora. The administration of metronidazole, approved by the WHO, is currently being used for trichomoniasis treatment. However, there is a great need for development of safe alternative drugs from natural products because of metronidazole’s adverse effects. In this investigation, bee venom effectively inhibited Trichomonas vaginalisgrowth in a concentration-dependent manner.

Neutrophils are the predominant inflammatory cells found in the vaginal discharges of patients infected with Trichomonas vaginalis. Although chemoattractants, such as leukotriene B(4) and interleukin-8 (IL-8), are found in the vaginal discharges of symptomatic trichomoniasis patients, little is known about the mechanism of how neutrophils accumulate or mediate initial inflammatory response after acute T. vaginalis infection. We examined IL-8 production in neutrophils activated by T. vaginalis and evaluated the factors involved in T. vaginalis adherence that might affect IL-8 production. When human neutrophils were stimulated with live trophozoites, T. vaginalis lysate, or T. vaginalis excretory-secretory products, the live trichomonads induced higher levels of IL-8 production than the lysate or products did. When live trichomonads were pretreated with various inhibitors of proteinase, microtubule, microfilament, or adhesin (which are all known to participate in the adherence of T. vaginalis to vaginal epithelial cells), IL-8 production significantly decreased compared with the untreated controls. Furthermore, an NF-kappaB inhibitor (pyrrolidine dithiocarbamate), a mitogen-activated protein (MAP) kinase (MEK) inhibitor (PD98059), and a p38 MAP kinase inhibitor (SB203580) significantly suppressed IL-8 synthesis in neutrophils. These results suggest that live T. vaginalis, particularly adherent trophozoites, can induce IL-8 production in neutrophils and that this action may be mediated through the NF-kappaB and MAP kinase signaling pathways. In other words, T. vaginalis-induced neutrophil recruitment may be mediated via the IL-8 expressed by neutrophils in response to activation by live T. vaginalis.

ABSTRACTNeutrophils are the predominant inflammatory cells found in the vaginal discharges of patients infected with Trichomonas vaginalis. Although chemoattractants, such as leukotriene B4and interleukin-8 (IL-8), are found in the vaginal discharges of symptomatic trichomoniasis patients, little is known about the mechanism of how neutrophils accumulate or mediate initial inflammatory response after acute T. vaginalisinfection. We examined IL-8 production in neutrophils activated by T. vaginalisand evaluated the factors involved in T. vaginalisadherence that might affect IL-8 production. When human neutrophils were stimulated with live trophozoites, T. vaginalislysate, or T. vaginalisexcretory-secretory products, the live trichomonads induced higher levels of IL-8 production than the lysate or products did. When live trichomonads were pretreated with various inhibitors of proteinase, microtubule, microfilament, or adhesin (which are all known to participate in the adherence of T. vaginalisto vaginal epithelial cells), IL-8 production significantly decreased compared with the untreated controls. Furthermore, an NF-κB inhibitor (pyrrolidine dithiocarbamate), a mitogen-activated protein (MAP) kinase (MEK) inhibitor (PD98059), and a p38 MAP kinase inhibitor (SB203580) significantly suppressed IL-8 synthesis in neutrophils. These results suggest that live T. vaginalis, particularly adherent trophozoites, can induce IL-8 production in neutrophils and that this action may be mediated through the NF-κB and MAP kinase signaling pathways. In other words, T. vaginalis-induced neutrophil recruitment may be mediated via the IL-8 expressed by neutrophils in response to activation by live T. vaginalis.

Park, H., Hong, K-M., Sakanari, J. A., Choi, J-H., Park, S-K., Kim, K-Y., Hwang, H-A., Paik, M-K., Yun, K-J., Shin, C-H., Lee, J-B., Ryu, J-S., Min, D-Y. 2001. Paragonimus westermani: Cloning of a cathepsin F-like cysteine proteinase from the adult worm. Experimental Parasitology98, 223 –227.

We have investigated the action of sodium nitrite and other nitrosyl complexes, such as sodium nitroprusside and Roussin's black salt, on the growth of metronidazole-sensitive and resistant strains of Trichomonas vaginalis and their hydrogenosomal enzymes. All three chemicals inhibited the growth of T. vaginalis: sodium nitrite at 8 mM, sodium nitroprusside at 1.2 mM and Roussin's black salt at 0.2 mM. Metronidazole-sensitive (KT9) and resistant (CDC85) isolates showed similar cytotoxicity against these molecules. Specific activities of pyruvate:ferredoxin oxidoreductase and hydrogenase and oxygen uptake rates were decreased in the T. vaginalis isolate treated with sodium nitrite and sodium nitroprusside. However, Roussin's black salt increased the specific activity of pyruvaterferredoxin oxidoreductase or hydrogenase in CDC85 or KT9 cells and increased the oxygen uptake rate in the KT9 isolate.