Since the molecular mechanisms of macrophage activation in response to interferon gamma (IFN-γ) are still not well defined we have investigated whether amiloride, a specific inhibitor of the Na+/H+ antiporter, had any effect on the IFN-γ-mediated potentiation of human monocyte and monocyte-derived macrophage capability to produce O−2 (respiratory burst). Here, we demonstrate that amiloride neither inhibits the capability of IFN-γ to activate the mononuclear phagocyte respiratory burst nor influences IFN-γ induction of steady-state mRNA levels for 2 components of the superoxide anion-generating enzyme system. On the contrary, we show that IFN-γ-enhanced expression of the HLA-DRα gene is significantly inhibited by amiloride (see also ref. 5). These data indicate that Na+/H+ antiporter stimulation by IFN-γ is not involved in the mechanism of activation of macrophage oxidative metabolism.
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