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Nitric Oxide Synthase Is Not a Constituent of the Antimicrobial Armature of Human Mononuclear Phagocytes

Schneemann, Markus ; Schoedon, Gabriele ; Hofer, Simone ; Blau, Nenad ; Guerrero, Lourdes ; Schaffner, Andreas

In: Journal of Infectious Diseases, 1993, vol. 167, no. 6, p. 1358-1363

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    Titre
    • Nitric Oxide Synthase Is Not a Constituent of the Antimicrobial Armature of Human Mononuclear Phagocytes
    Auteur
    • Schneemann, Markus. Clinical Mycology Laboratory, Division of Infectious Diseases, Department of Medicine, University of Zurich Medical School, Switzerland
    • Schoedon, Gabriele. Clinical Mycology Laboratory, Division of Infectious Diseases, Department of Medicine, University of Zurich Medical School, Switzerland
    • Hofer, Simone. Clinical Mycology Laboratory, Division of Infectious Diseases, Department of Medicine, University of Zurich Medical School, Switzerland
    • Blau, Nenad. Clinical Mycology Laboratory, Division of Infectious Diseases, Department of Medicine, University of Zurich Medical School, Switzerland
    • Guerrero, Lourdes. Clinical Mycology Laboratory, Division of Infectious Diseases, Department of Medicine, University of Zurich Medical School, Switzerland
    • Schaffner, Andreas. Clinical Mycology Laboratory, Division of Infectious Diseases, Department of Medicine, University of Zurich Medical School, Switzerland
    Type de document
    • Postprint
    Langue
    • Anglais
    Publié dans
    • Journal of Infectious Diseases, 1993, vol. 167, no. 6, p. 1358-1363. The University of Chicago Press
    Autre version électronique
    Classification
    • Santé
    Identifiant OAI-PMH
    • oai:doc.rero.ch:297283
    Summary
    Nitric oxide synthase (NOS) has received immense interest as an antimicrobial and antitumoral effector system of mononuclear phagocytes from rodents. Because there is increasing doubt that an analogous system exists in human macrophages, NOS was reexamined in these cells. Under tightly controlled conditions, with murine macrophages as positive controls, human macrophages failed to secrete nitric oxide <0.1µmol/106 cells/24 h), even after activation with endotoxin, intcrferon-γ, granulocyte-macrophage colony-stimulating factor, tumor necrosis factor- a, bacteria, or proliferating lymphocytes. The discrepancy between murine and human macrophages depended on neither the anatomic source (blood, peritoneum), the agent used for activation, nor the duration of activation. NOS activity was paralleled by metabolization of L-arginine to L-citrulline. Exogenous tetrahydrobiopterin, an essential cofactor of NOS not synthesized by human macrophages, did not support NOS activity in human macrophages. Also, no NOS activity was found in cellular subfractions of human macrophages. It appears that in humans, the inducible high-output NOS is not conserved as an antimicrobial system of macrophages