Further evidence for the procidin function of C3

It was found that heat-inactivated serum supported phagocytosis, but did not promote oxygen consumption or killing of Candida, by human polymorphonuclear leucocytes (PMNs). It was also established that C3 is required for activation of the PMN candidacidal related mechanisms of superoxide anion generation and iodination. Addition of purified C3 to C3 deficient serum restored phagocytic killing. Further evidence for C3 involvement in Candida killing was obtained from studies of PMN ingestion and killing in the presence of trypan blue or heparin. Trypan blue, which antagonises C3 receptors, prevented efficient killing, as did heparin, which affects C3 conversion in normal serum. From these results it is evident that phagocytic killing is not an obligatory consequence of ingestion. The findings also indicate that killing by PMNs is dependent upon the interaction of humoral factors, termed procidins, with receptors responsible for initiation of microbicidal mechanisms. Activation products of C3 may stimulate phagocytic killing by engagement of their counterpart receptors on PMNs.