Copper Regulation of Macrophage Eicosanoid and Cyclic-AMP Synthesis

Copper has been shown to be anti-inflammatory in a number of acute and chronic models of inflammation, as assessed by oedematous changes (1). However, its effect on other parameters associated with chronic reactions, e.g. tissue damage and growth, are equivocal (2, 3). Copper can effect a number of reactions known to occur at the inflammatory site. For example it can inhibit chondrocyte growth and mitogen induced lymphocyte proliferation and it is necessary for lysyl oxidase activity and hence collagen synthesis (4–6). Copper could therefore, stimulate tissue repair and limit immune activation, and the associated stimulation of other cell types, at the inflammatory site. The macrophage plays an important role in regulating chronic inflammations releasing not only lysosomal enzymes and active oxygen species which could damage tissue but also secreting mediators such as interleukin-1, which activates the immune system (7, 8).