Macrophages from experimental wounds in rats were tested for their capacity to generate reactive oxygen intermediates. Measurements of superoxide and H₂O₂ release, O₂-dependent lucigenin chemiluminescence, oxygen consumption, hexose monophosphate shunt flux, and NADPH oxidase activity in cell lysates indicated, at best, the presence of a vestigial respiratory burst response in these cells. The inability of wound cells to release O₂ was not rekindled by priming with endotoxin or interferon- in vivo or in vitro. NADPH oxidase activity in a cell-free system demonstrated that wound macrophage membranes, but not their cytosols, were capable of sustaining maximal rates of O₂ production when mixed with their corresponding counterparts from human neutrophils. Immune detection experiments showed wound macrophages to be particularly deficient in the cytosolic component of the NADPH oxidase p47-phox. Addition of recombinant p47-phox to the human neutrophil-cell membrane/wound macrophage cytosol cell-free oxidase assay, however, failed to support O₂ production. Present findings indicate an unexpected deficit of wound macrophages in their capacity to generate reactive oxygen intermediates.

rodent; monocytes; inflammation

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