Amiloride does not influence the capability of interferon gamma to potentiate superoxide anion and hydrogen peroxide release by human mononuclear phagocytes.

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.