Attempts to characterize the mechanisms involved in mycobacterial growth inhibition by gamma-interferon-activated bone marrow macrophages.
Bone marrow-derived murine macrophages are able to inhibit the growth of Mycobacterium bovis and of some strains of M. tuberculosis after stimulation with either recombinant gamma interferon (rIFN-gamma) or lymphokines from antigen-specific T-cell clones. To elucidate the mechanism(s) involved in antimycobacterial activity, macrophages were infected with M. bovis in the presence of agents thought to influence the antimicrobial effects of phagocytes. Scavengers of toxic oxygen metabolites failed to influence the capacity of IFN-gamma-activated bone marrow macrophages to inhibit the growth of M. bovis. Suramin slightly affected mycobacterial growth in IFN-gamma-activated macrophages, and chloroquine markedly induced growth inhibition of M. bovis in unstimulated macrophages. We conclude that growth inhibition of M. bovis by IFN-gamma-activated macrophages is an oxygen-independent process.
D000818:Animals; D000898:Antibiosis / Q000187:drug effects; D001854:Bone Marrow Cells; D002082:Butylamines / Q000494:pharmacology; D002738:Chloroquine / Q000494:pharmacology; D005260:Female; D005609:Free Radicals; D007371:Interferon-gamma / Q000494:pharmacology*; D008262:Macrophage Activation / Q000187:drug effects; D051379:Mice; D008810:Mice, Inbred C57BL; D009163:Mycobacterium bovis / Q000187:drug effects / Q000254:growth & development* / Q000378:metabolism; D009169:Mycobacterium tuberculosis / Q000187:drug effects / Q000254:growth & development* / Q000378:metabolism; D010100:Oxygen / Q000633:toxicity; D011099:Polyglutamic Acid / Q000494:pharmacology; D011994:Recombinant Proteins / Q000494:pharmacology; D013498:Suramin; D013748:Tetracaine / Q000494:pharmacology
D002082:Butylamines; D005609:Free Radicals; D011994:Recombinant Proteins; D013748:Tetracaine; D011099:Polyglutamic Acid; D013498:Suramin; D007371:Interferon-gamma; D002738:Chloroquine; C036355:tributylamine; D010100:Oxygen