Oxford University Press (OUP), FEMS Immunology and Medical Microbiology, 1(21), p. 11-17
DOI: 10.1016/s0928-8244(98)00025-x
Oxford University Press (OUP), FEMS Immunology and Medical Microbiology, 1(21), p. 11-17, 1998
DOI: 10.1111/j.1574-695x.1998.tb01144.x
Full text: Download
Monocytes/macrophages from human immunodeficiency virus (HIV)-infected patients had a defect in their ability to kill Rhodococcus equi in vitro, as compared with healthy HIV-seronegative individuals. Virulent and avirulent R. equi strains isolated from humans and horses showed no significant intracellular replicative differences within both HIV-positive and -negative monocytes/macrophages. Infection with R. equi induced the production of nitric oxide (NO) by monocytes/macrophages from healthy individuals, but not by cells from HIV-positive patients. The NO formation was significantly inhibited by L-N-G-monomethyl arginine and arginase. However, neither competitive inhibition of NO synthesis from L-arginine with L-NMMA nor depletion of arginine with arginase altered the killing activity of human monocytes/macrophages against R. equi, thus suggesting that L-arginine:NO pathway is not required for the intracellular antirhodococcal mechanisms of human monocytes/macrophages. (C) 1998 Published by Elsevier Science B.V.