Phagocytosis of Listeria monocytogenes by mouse peritoneal macrophages in vitro only occurs in the presence of fresh mouse serum. Opsonic activity of normal mouse serum for listeria proved to be dependent on activation of the third component of mouse complement via the alternative pathway. This could be concluded from the following facts: heat inactivation as well as zymosan treatment of normal mouse serum strongly reduced its opsonic activity; EDTA, but not EGTA, inhibited opsonic acitivity and treatment of mice with cobra venom factor caused a sharp decline in the opsonic activity of their serum for L. monocytogenes. The strong activation of mouse C3 via the alternative pathway by listeria, resulting in deposition of C3b molecules on the listerial cell wall, promotes uptake of these microorganisms by mouse macrophages, presumably via their C3b receptors. The terminal complement components (C5-C9) do not appear to be essential for opsonization of listeria, since the opsonic activity of serum from C5-deficient mice was identical to that of normal mouse serum.
It is speculated that the present findings offer a possible explanation for the well-known fact that, even in non-immunized mice, listeria, injected by either the intravenous or intraperitoneal route, are rapidly cleared by the mononuclear phagocyte system and, thus, why these intracellular parasites become localized so easily in mononuclear phagocytes.