Lymphokines and bacteria, that induce tumoricidal activity, trigger a different secretory response in macrophages.

The abilities of various macrophage-activating agents to trigger tumoricidal activity and/or the secretion of prostaglandin E2 (PGE2), interleukin 6 (IL 6) and transforming growth factor beta (TGF beta) in bone marrow-derived mononuclear phagocytes (BMM phi) in vitro were comparatively assessed. Induction of tumoricidal activity by lymphokines, that is only short-lived, was not associated with enhanced secretion of these activities by BMM phi; in contrast, incubation with heat-killed facultative intracellular bacteria resulted in persisting tumoricidal activity and in marked enhancement of the secretion of IL 6 and PGE2, but not of TGF beta activity. These findings support the concept that the pattern of the secretory response induced in macrophages by lymphokines differs from that triggered by bacteria and that the rapid decay of lymphokine-induced tumoricidal activity is not due to autocrine macrophage deactivation mediated by one of these agents alone.