Open AccessRhodococcus equi infection of monocytes/macrophages from human immunodeficiency virus (HIV)‐infected patients and healthy individuals: evaluation of intracellular killing and nitric oxide production
Author(s) -
Vullo Vincenzo,
Mastroianni Claudio M,
Lichtner Miriam,
Mengoni Fabio,
D'Agostino Claudia,
Forcina Gabriele,
Corpolongo Angela,
Delia Salvatore
Publication year - 1998
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.1998.tb01144.x
Subject(s) - rhodococcus equi , arginase , biology , intracellular , macrophage , monocyte , nitric oxide , microbiology and biotechnology , arginine , virology , virus , in vitro , immunology , virulence , biochemistry , amino acid , gene , endocrinology
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.