Delayed hypersensitivity reactions to Listeria monocytogenes in rats decomplemented with cobra factor and in C5-deficient mice.

The in vivo effect of cobra factor (CoF), the complement-activating protein of cobra (Naja naja) venom, was investigated, using quantifiable assays for localization of labelled donor lymphoblasts and of host macrophages in intraperitoneal and subcutaneous sites of injection of antigens from Listeria monocytogenes. Both commercially available (Cordis) and highly purified CoF impaired these inflammatory responses, suggesting that the complement-activating protein was itself responsible rather than lymphocytotoxic or other contaminants. CoF had no measurable effect on lymphoblast localization during the first 7 hr, and only a slight effect at 24 hr, whereas macrophage accumulation was reduced by about 50% at 24 hr. This suggests that CoF treatment affected non-specific components of the early inflammatory reaction but had little or no effect on the subsequent immunospecific reaction. The effect of CoF on macrophages may be direct, or via depletion of complement components acting on macrophages, such as factor B and/or C3 or fragments thereof. It does not seem to involve the terminal complement components, C5--C9, since neither delayed-type hypersensitivity (DTH) nor cellular resistance to Listeria was reduced in C5-deficient mice when compared with C5-sufficient congenic controls.