Abstract
Studies performed in vitro have demonstrated that C3 acts as an opsonin when activated to C3b and fixed to bacteria. In order to investigate the significance of C3 as an opsonin in vivo the following experiments were performed in normal, nonimmune mice. Mice were totally depleted of serum C3, as measured in a hemolytic assay, by the injection of cobra venom factor(CoVF). Concurrent with the C3 depletion their serum opsonizing activity decreased to a level less than 20% of normal. When mice were challenged with an intraperitoneal injection of pneumococci(Pn) immediately after the CoVF treatment, the LD50 was 1.8 × 106 as compared to 6.8 × 107 in saline treated control animals (P<0.05). When the CoVF was given only 6 hours after the Pn challenge the LD50 was the same as in the control mice. If Pn were preopsonized in vitro with nonimmune mouse serum and then injected into CoVF treated animals, the LD50 was the same as that in control animals. These studies demonstrate that there is a biologically significant in vivo role for C3 as an opsonin in the nonimmune host's defense against bacterial infection and that that role is most significant in the early stages of bacterial invasion.
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