GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR IS NOT INVOLVED IN PRODUCTION OF REACTIVE NITROGEN INTERMEDIATES BY OR TOXOPLASMASTATIC ACTIVITY OF GAMMA-INTERFERON-ACTIVATED MURINE MACROPHAGES

The induction of reactive nitrogen intermediates (RNI) and toxoplasmas tatic activity of murine macrophages by recombinant gamma interferon ( rIFN-gamma) is mediated by an autocrine pathway involving tumor necros is factor alpha (TNF-alpha). To investigate whether cytokines other th an TNF-alpha play a role in the activation of these effector functions , granulocyte-macrophage colony-stimulating factor (GM-CSF) was studie d. Recombinant GM-CSF (rGM-CSF) could stimulate peritoneal macrophages , since this cytokine stimulated the production of prostaglandin E(2) by these cells. However, rGM-CSF did not induce either the release of RNI by or the toxoplasmastatic activity of macrophages. rGM-CSF in com bination with various concentrations of rIFN-gamma did not enhance the se effector functions more than rIFN-gamma alone. Furthermore, neutral ization of endogenously produced GM-CSF by monoclonal antibodies did n ot affect the release of RNI by or the toxoplasmastatic activity of rI FN-gamma-activated macrophages. Together these results indicate that G M-CSF is not involved in RNI production by and toxoplasmastatic activi ty of IFN-gamma-activated murine macrophages.