Priming of human alveolar macrophages and blood monocytes for superoxide anion release by interferons and lipopolysaccharide.

Biological agents such as the interferons (IFNs) or lipopolysaccharides (LPSs) can prime phagocytic cells to generate increased amounts of oxygen metabolites upon exposure to various stimuli. The priming of human peripheral blood monocytes and alveolar macrophages (AM) by recombinant IFN-beta ser (rIFN-beta ser) and rIFN-gamma for an enhanced respiratory burst was compared. Both rIFN-beta ser and rIFN-gamma increased phorbol myristate acetate-stimulated superoxide anion generation by AM in a dose-dependent fashion. rIFN-beta ser was capable of priming AM for an enhanced superoxide anion release nearly as well as rIFN-gamma. In contrast, rIFN-beta ser was much less effective as a priming agent for monocytes when compared to either its effect on AM or to the priming effect of rIFN-gamma on monocytes. The respiratory burst of IFN-exposed AM was not inhibited by co-incubation with low concentrations of LPS. However, the ability of IFN to augment superoxide anion release by cells simultaneously exposed to LPS in comparison to superoxide anion generation by cells exposed to LPS only was attenuated.