Macrophages can be activated to produce reactive oxygen intermediates, such as superoxide anion (O2-), which are responsible for intracellular killing of pathogenic microbes. Treatment with either native or recombinant somatotropin augmented the production of O2- by both peripheral blood-derived and alveolar macrophages stimulated with opsonized zymosan in vitro. This effect was abolished by prior treatment with an antibody specific for somatotropin. When either native or recombinant porcine somatotropin or native rat somatotropin was administered to hypophysectomized rats in vivo, activation of peritoneal macrophages, as measured by release of O2- in response to opsonized zymosan, was equivalent to that of macrophages from rats primed with the macrophage-activating factor interferon-gamma. Priming of macrophages in vivo was observed at physiologically relevant doses of somatotropin that caused a 10 to 40 percent increase in growth rate. Priming of mononuclear phagocytes for augmented production of reactive oxygen metabolites is a newly defined property of somatotropin.

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