The role of arachidonic acid metabolites in mononuclear phagocytic cell interactions.

Abstract

Numerous investigations support the theory that arachidonic acid metabolites play a critical role in dictating the progression of chronic immune reactions. With regard to macrophage-mediated inflammatory responses, enzymatic oxygenation of arachidonic acid via the lipoxygenase or cyclooxygenase pathway can result in the production of compounds that may potentiate or suppress the inflammatory lesion. We recently have presented data demonstrating that lipoxygenase derived leukotriene B4 and C4 can induce the release of IL-1 by macrophages, while PGE2 and PGI2 can suppress the production of IL-1. Macrophages are central to the induction of immune responses and the progression of chronic inflammatory reactions. Therefore, an understanding of the role that macrophage-derived arachidonic acid metabolites play in the initiation, maintenance, and resolution of chronic immune responses is essential. As shown in Figure 3, there are a number of chemical signals that occur between macrophages and lymphocytes that are critical for immune cell communication. The investigations described above have demonstrated that the macrophage may regulate the production and expression of any or all of these signals, such that the inflammatory response is potentiated, sustained, suppressed, or resolved. A better comprehension of the activity of these potent arachidonate derivates will undoubtedly aid in the therapeutic manipulation of inflammatory disease.