The macrophage adherence phenomenon: its relationship to prostaglandin E2 and superoxide anion production and changes in transmembrane potential.

Mononuclear phagocytes are undoubtedly the sine qua non of chronic inflammatory reactions. This is demonstrated by their unique ability to function as phagocytic, secretory, or effector cells during the course of an immune event. Although macrophages can perform a variety of immune tasks, their ability to function appropriately is dependent upon the mode of elicitation, the stimulus under investigation, the source of the macrophages (peritoneal, alveolar, etc.), and whether the macrophages are monolayers or in suspension. We have examined the relationship between adherent and non-adherent elicited peritoneal macrophages in terms of prostaglandin E2 (PGE2) and superoxide anion (O2-) production; in addition, we have studied these elicited macrophages in suspension for their ability to undergo transmembrane potential changes in response to several stimuli. Non-adherent, elicited peritoneal macrophages demonstrated an increase in basal PGE2 production, and were refractory to particulate stimulus. After monolayer formation, basal PGE2 levels dropped and the cells could respond to both soluble and particulate stimuli. Only adherent macrophages could respond to a specific challenge and synthesize O2-. Both O2- production and depolarization of the transmembrane potential were suppressed in cells in suspension. Furthermore, both exogenous PGE2 and supernatant from macrophages in suspension could modulate O2- production by PMA challenged macrophages monolayers. These studies indicate that PGE2 may modulate macrophage function and dictate activity as macrophages go from the non-adherent to adherent state.