Lymphokine-mediated microbistatic mechanisms restrict Chlamydia psittaci growth in macrophages.

The obligate intracellular procaryote Chlamydia psittaci replicated in cultures of macrophages taken from the peritoneal cavities of unstimulated or thioglycollate-elicited A/J mice. When treated with supernatant fluids (lymphokines) from C. psittaci-immune mice spleen cells that were stimulated for 24 hr in vitro by the mitogen concanavalin A, resident macrophages supplemented with heart infusion broth (8 mg/ml) and elicited macrophages markedly suppressed intracellular chlamydial development. Uptake of the parasites was unaffected by LK-activated macrophages. The LK-induced inhibition was a static rather than a cidal effect. Chlamydial replication was detected 24 to 41 hr after removal of LK and infection with C. psittaci. Evidence that intermediates of oxygen metabolism did not contribute to the microbistatic process in either resident or elicited macrophages was provided by the inability of exogenous catalase, deprivation of glucose, or pretreatment with phorbol myristate acetate (PMA) to reverse LK-induced inhibition of parasite replication.