The role of nitric oxide as an effector of macrophage-mediated cytotoxicity against Trichomonas vaginalis.

Abstract

The purpose of this study is to determine whether nitric oxide is involved in the extracellular killing of Trichomonas vaginalis by mouse (BALB/c) peritoneal macrophages and RAW264.7 cells activated with LPS or rIFN-gamma and also to observe the effects of various chemicals which affect the production of reactive nitrogen intermediates (RNI) in the cytotoxicity against T. vaginalis. The cytotoxicity was measured by counting the release of [3H]-thymidine from labelled protozoa and NO2- was assayed by Griess reaction. NG-monomethyl-L-arginine (L-NMMA), NG-nitro-L-arginine methyl ester (NAME) and arginase inhibited cytotoxicity to T. vaginalis and nitrite production by activated mouse perioneal macrophages and RAW 264.7 cells. The addition of excess L-arginine competitively restored trichomonacidal activity of macrophages. Exogenous addition of FeSO4 inhibited cytotoxicity to T. vaginalis and nitric products of macrophages. From above results, it is assumed that nitric oxide plays an important role in the host defense mechanism of macrophages against T. vaginalis.