Opsonized Legionella Pneumophila Multiplies in Monocytes

The fate of an intracellular pathogen in mononuclear phagocytes appears to be an important determinant of the capacity of the pathogen to cause disease. Antibody against the pathogen can markedly alter the intracellular fate of the pathogen in mononuclear phagocytes; such an effect of antibody is reflected in vivo by enhanced resistance to infection of animals that have been passively immunized with hyperimmune serum. Under these conditions, the specific immunity expressed by these animals results from the presence of antibody and not from the presence of antigensensitive leukocytes. For example, antibody inhibited the intracellular multiplication of the obligate intracellular parasite Rickettsia mooseri in cultured human monocytes and rendered the organism susceptible to killing by these monocytes (1); paralleling this in vivo, the same antibody protected passively immunized mice against an otherwise lethal infection from R. mooseri ([1]; and C. L. Wisseman, Jr. Personal communication.). Similarly, human and mouse antitoxoplasma antibody rendered the obligate intracellular parasite Toxoplasma gondii incapable of multiplying in cultured human monocytes (2) and mouse peritoneal macrophages (3), respectively; mouse anti-toxoplasma antibody protected passively immunized mice from lethal infection with T. gondii (4). With other intracellular pathogens, antibody does not significantly inhibit their multiplication in cultured leukocytes; this is reflected in vivo by a failure of antibody to protect passively immunized animals from infection. For example, immune mouse serum did not inhibit the multiplication of the facultative intracellular bacterium Listeria monocytogenes in cultured mouse peritoneal macrophages (5); and immune mouse serum did not protect mice from infection with L. monocytogenes (6). Similarly, antibody did not inhibit the multiplication of the facuhative intracellular bacterium Mycobacterium tuberculosis in cultured mouse, rabbit, or guinea pig peritoneal macrophages (7-9); and immune mouse serum did not influence the survival of mice nor did immune guinea pig serum influence the course of infection in guinea pigs when these animals were challenged with M. tuberculosis (10, 11). In all these studies, there is a correlation between the capacity of antibody to inhibit intracellular infection of