Macrophages from experimental wounds in rats were tested for their capacity
to generate reactive oxygen intermediates. Measurements of superoxide and
H2O2, release, O-2(-)-dependent lucigenin chemiluminescence, oxygen consump
tion, hexose monophosphate shunt flux, and NADPH oxidase activity in cell l
ysates indicated, at best, the presence of a vestigial respiratory burst re
sponse in these cells. The inability of wound cells to release O-2(-) was n
ot rekindled by priming with endotoxin or interferon-gamma in vivo or in vi
tro. NADPH oxidase activity in a cell-free system demonstrated that wound m
acrophage membranes, but not their cytosols, were capable of sustaining max
imal rates of O-2(-) production when mixed with their corresponding counter
parts from human neutrophils. Immune detection experiments showed wound mac
rophages to be particularly deficient in the cytosolic component of the NAD
PH oxidase p47-phox. Addition of recombinant p47-phox to the human neutroph
il-cell membrane/wound macrophage cytosol cell-free oxidase assay, however,
failed to support O-2(-) production. Present findings indicate an unexpect
ed deficit of wound macrophages in their capacity to generate reactive oxyg
en intermediates.