The development of non-specific immunosuppression during the infection of different strains of mice with three mycobacterial species was evaluated by studying the immune response to a heterologous antigen (sheep red blood cells) and comparing it with the induction of non-specific resistance to a Listeria monocytogenes challenge. It was shown that early (at 15 days) immunosuppression developed in Mycobacterium avium-susceptible mouse strains infected with a high inoculum dose [2.5 x 10(8) colony forming units (CFU)] of virulent M. avium but not in resistant mice infected with a similar inoculum nor in susceptible mice infected by a smaller inoculum dose (2.5 x 10(6) CFU). In the latter case it developed only during the second month of infection and was of smaller magnitude. An inoculum of M. avium of attenuated virulence did not induce immunosuppression. M. lepraemurium induced a late immunosuppression, which occurred when extensive bacterial proliferation had already taken place. The non-pathogenic M. bovis BCG induced immunosuppression in C57BL/6 mice. The results do not establish a correlation between the development of generalized immunosuppression and susceptibility to infection. It could be seen that the early immunosuppression was observed in those situations where there was extensive macrophage activation as shown by the development of non-specific resistance to a listeria challenge. The late immunosuppression was observed when bacterial proliferation was extensive.

A major role has been recently ascribed to the neutrophil in the resistance to infection by Listeria monocytogenes (L. monocytogenes). Here we evaluated whether such neutrophils played a role in the non‐specific resistance to listeriosis that develops in hosts infected by mycobacteria. We found that the depletion of neutrophils completely abrogated the resistance conferred by the activated macrophages induced during the mycobacterial infection. The lack of killing by activated Kupffer cells and the visualization of bacteria proliferating inside peritoneal macrophages in neutrophil‐depleted mice allowed us to postulate a role for the cooperation between neutrophils and macrophages in the killing of L. monocytogenes. We also found listerial proliferation in hepatocytes of neutrophil‐depleted, mycobacteria‐infected mice showing that the neutrophils may be involved in the control of listeria infection of parenchymal cells.