Human macrophages may normally be "primed" for a strong oxygen radical response.

Human blood monocytes, peritoneal macrophages and milk macrophages, when initially isolated, displayed a vigorous release of superoxide anion (0-2), following stimulation with phorbol myristate acetate (PMA). This result contrasts with behavior of mouse peritoneal macrophages, which produce a weak 0-2 response, unless the macrophages are activated by infection or are elicted by injection of inflammatory agents. Treatment of mouse cells in vitro with bacterial products such as lipopolysaccharide (LPS) or muramyl dipeptide (MDP) also "primes" them for a high 0-2 response. Exposure of human macrophages to LPS or MDP for 16 h failed to enhance their 0-2 response. Thus the human cells appeared to be already "primed" for a vigorous oxygen radical response. In this respect, human cells resembled mouse peritoneal macrophages that have been "activated" by infection. These results suggest that MDP or other macrophage "activators" may offer less protection against infection in normal humans than they do in mice.