Legionella pneumophila is an important cause of human pneumonia. Epidemiologic evidence suggests that exposure to the bacterium is common, but overt disease is not. The cellular and humoral immune mechanisms responsible for controlling a legionella infection have not been determined. Exposure of human and animal cells to the bacterium in vitro suggests that the bacterium is an intracellular parasite. The bacterium was able to multiply within normal alveolar macrophages and was inhibited but not killed by activated monocytes and polymorphonuclear leukocytes. Addition of immune serum increases the phagocytosis of L. pneumophila without affecting the intracellular growth rate of the bacterium. The bacterium is, therefore, capable of circumventing several important defense mechanisms of a phagocyte. I plan to study several mechanisms which may be involved in the intracellular survival of L. pneumophila. I will use a recently developed tissue culture system to study the mode of entry of L. pneumophila into a phagocyte and the interaction of the bacterium (both virulent and avirulent) with the microbicidal mechanisms of a host cell. The intracellular microbicidal mechanisms which will be studied will be the exidative burst and phagosome-lysosome fusion. The effect of an immune response (either humoral or cellular) on the interaction of L. pneumophila with the phagocytic, microbicidal system will be addressed. Results from this study will serve as a basis for future investigations into the molecular aspects of the interaction of L. pneumophila and its host cell.
| Elliott, J A; Winn Jr, W C (1986) Treatment of alveolar macrophages with cytochalasin D inhibits uptake and subsequent growth of Legionella pneumophila. Infect Immun 51:31-6 |
