The interactions of cells of Nocardia asteroides GUH-2 during different stages of growth with cultured macrophages obtained from the lungs of nonimmunized and immunized rabbits were studied. The nocardial cells from all stages grew intracellularly in "normal" alveolar macrophages; however, log-phase cells increased in numbers more rapidly than did stationary-phase cells. Macrophages obtained from the lungs of specifically immunized rabbits effectively inhibited the growth of stationary-phase cells but only temporarily retarded the growth of log-phase organisms. Specific antiserum added to the nocardial cells before incubation with presensitized macrophages caused enhanced phagocytosis and inactivation of the log-phase cells but had no effect on the fate of the stationary-phase nocardia. In addition, it was fo-nd that log-phase cells were phagocytized less effectively by normal macrophages than were the stationary-phase cells, and log-phase cells were more toxic to the macrophage monolayer. From these data we conclude that secondarily induced macrophages play a major role in host resistance to pulmonary nocardial infections, and antibody may be important for effective host resistance to the filamentous form of N. asteroides. Since the nocardia were able, with time, to overcome these effects, it appears that additional host factors (such as T-lymphocytes) must be involved in an effective host response to N. asteroides.