Inability of tumour cells to elicit the respiratory burst in cytotoxic, activated macrophages.
Activated macrophages from Corynebacterium parvum-treated mice are cytotoxic to non-antibody-coated tumour cells and have an augmented respiratory burst potential when compared to resident macrophages. We have investigated the possible involvement of the respiratory burst as an effector mechanism in this type of tumour killing. Scavengers of toxic metabolites of oxygen such as catalase, superoxide dismutase, 2,3-dihydroxybenzoate, ethanol, and cytochrome c did not inhibit macrophage cytotoxicity in this system. To investigate whether or not neoplastic cells stimulate the macrophage respiratory burst, we exposed activated macrophages to viable tumour cells and monitored macrophage superoxide anion production, chemiluminescence, and hexose monophosphate shunt activity. None of these indicators of the macrophage respiratory burst was stimulated by the tumour cells towards which the macrophages were cytotoxic. The data suggest that the macrophages burst is not utilized as an effector mechanism in the non-antibody-mediated macrophage tumour cytotoxicity reaction.
D000818:Animals; D003602:Cytotoxicity, Immunologic / Q000187:drug effects; D005260:Female; D006600:Hexosephosphates / Q000378:metabolism; D008163:Luminescent Measurements; D008262:Macrophage Activation; D008264:Macrophages / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism; D051379:Mice; D008809:Mice, Inbred C3H; D010101:Oxygen Consumption / Q000187:drug effects; D011425:Propionibacterium acnes / Q000276:immunology; D013539:Simian virus 40; D014412:Tumor Virus Infections / Q000276:immunology*
D006600:Hexosephosphates