Thermal injury-induced enhancement of oxidative metabolism by mononuclear phagocytes.

C57BL/6 female mice were subjected to full-thickness scald thermal injuries covering 25% of their total body surface areas, and thioglycollate-elicited peritoneal macrophages were isolated 4 days later. Macrophages from burned mice displayed a 2-fold increase in phorbol ester-stimulated superoxide production, whereas superoxide production in response to zymosan or immune complexes was unaltered. Maximal levels of superoxide production by thermal injury macrophages were comparable for all stimuli. Reduction of injury size to 12.5% total body surface area abrogated the enhancement of superoxide production. Protein kinase C activity and protein phosphorylation was not altered after thermal injury. These results indicate that the enhancement of macrophage-oxidative metabolism after thermal injury is independent of changes in reduced nicotinamide adenine dinucleotide phosphate oxidase or protein kinase C activity and may in part explain the increased susceptibility to multiple organ failure after this form of trauma.