Polymorphonuclear neutrophils (PMN) from patients with chronic granulomatous disease (CGD), control patients with a variety of infections (inf. PMN) and PMN from one individual deficient in myeloperoxidase (MPO-def) were examined for phagocytosis in paired studies with normal healthy controls. Hyper-phagocytic activity was observed in PMN from 10 CGD patients and 12 infected patients as well as the patients with MPO deficiency. Normal PMN treated with sodium azide were also markedly more phagocytic than normal untreated PMN. Exogenously generated H2O2 caused a dramatic drop in phagocytosis by CGD and normal PMN while having no effect on MPO-Def. PMN. The H2O2 scavenger, catalase, also enhanced phagocytic activity in normal PMN. Thus, MPO and H2O2 both play a role in regulating PMN phagocytosis. This effect appears to be mediated by regulation of the PMN Fc receptor since attachment of IgG coated particles, but not C3b coated particles, is also abrogated in normal PMN. We showed previously that adhered cultured monocytes bind particles coated with the C3 degradation fragment, C3d, under certain conditions of activation and differentiation. We have also shown that, like the fragments C3b and iC3b, C3d enhances IgG mediated phagocytosis. Now we have clarified that the receptor involved in C3d binding is the iC3b receptor, CR3. Apparently monocyte CR3 expression changes in culture, allowing this receptor to interact with the C3d moiety of the C3 molecule.
