Copper Metabolism in Isolated Macrophages: Regulator of Immunity and Inflammation

Copper is essential for the proper functioning of immune cells and participates in diverse biochemical processes. The maintenance of copper ion homeostasis is critical for normal host physiology, while dysregulation of copper metabolism is closely linked to various diseases. Emerging evidence indicates that disease-associated elevations in copper levels significantly enhance macrophage functions, including the expression of inflammatory cytokines, phagocytosis, and bactericidal activity. As key innate immune cells, macrophages not only eliminate invading pathogens but also contribute to immune regulation, tissue repair, and angiogenesis. In this review, we summarize current knowledge of copper transport and homeostatic mechanisms in macrophages and highlight how copper regulates their antimicrobial activity, inflammatory responses, and reparative functions. A deeper understanding of these mechanisms may provide new insights into therapeutic strategies targeting macrophage regulation through copper metabolism in the context of infectious and inflammatory diseases.