Growth hormone is a human macrophage activating factor. Priming of human monocytes for enhanced release of H2O2.

Although many effects of growth hormone (GH) and related factors upon the immune system have been demonstrated, few studies have examined the capacity of these factors to modulate human monocyte function in vitro. Assaying a range of mediators, only GH and prolactin (PRL), at 0.3 to 1.0 micrograms/ml, and growth hormone-releasing hormone (GRH) at very high doses, primed monocytes for enhanced hydrogen-peroxide production (H2O2) in response to PMA. GH-induced priming was not caused by endotoxin, nor by production of lymphokines such as IFN-gamma. Exogenous insulin-like growth factor-I (IGF-I), alone or in combination with GH, was without effect, making it unlikely that GH mediates its effects on monocytes via an autocrine/paracrine action of IGF-I. Monocytes specifically bound radiolabeled GH and contained mRNA for the GH receptor and, in some donors, the PRL receptor. Therefore, GH probably exerts its effects as a human macrophage-activating factor through either GH or PRL receptors, without requiring production of IGF-I.