Human Macrophages May Normally be “Primed” for a Strong Oxygen Radical Response
In previous work we showed that macrophages must produce oxygen radicals in order to kill pathogenic organisms (1). Oxygen radical production by mouse peritoneal macrophages could be enhanced at least ten-fold if the macrophages were previously “activated”. (Throughout this paper we use the term “activated” to mean “primed to release optimal amounts of O 2 − when stimulated”). Macrophages were activated either by infecting the animals with Mycobacterium bovis, strain BCG, or by injecting them with bacterial lipopolysaccharide (LPS) or muramyl dipeptide (MDP) (2, 3). Cultured macrophages could also be activated in vitro by addition of LPS or MDP to the cultures (4). Treatment with LPS or MDP enhanced the ability of cultured macrophages to kill bacteria and fungi in vitro (1, 3). Treatment of mice with MDP in vivo enabled them to resist an otherwise lethal challenge infection with Klebsiella pneumoniae or Candida albicans (3, 5).
KeywordsPeritoneal Macrophage Phorbol Myristate Acetate Human Macrophage Phorbol Myristate Acetate Mouse Peritoneal Macrophage
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