Iron and Copper

The effect of iron (Fe) on immunocompetence is not as clear as that of Zn; however, generally speaking, an imbalance in Fe intake either too much or too little decreases immunity. One of the acute responses induced by infection is hypoferremia. The inflammatory cytokines released by activated macrophages cause Fe to be sequestered. Because Fe is a rate-limiting nutrient for the growth of several pathogenic microorganisms, its removal from blood and temporary storage in compartments that are not accessible to pathogens is considered part of the host defense. Iron-binding proteins chelate the most Fe; however, supplementation can saturate these proteins, leaving excess Fe available to pathogens.

Copper (Cu) status is determined primarily by the plasma concentration of the acute-phase protein ceruloplasmin. The inflammatory cytokines induce synthesis of cerulo-plasmin. Therefore, whereas infection decreases circulating Fe, it increases circulating Cu. The increase in plasma Cu may be to enhance lymphocyte responses because Cu deficiency reduces production of IL-2 a cytokine that acts in an autocrine manner to promote T-cell proliferation. To our best knowledge, there have been no studies clearly demonstrating that the Cu required for optimum immunity is higher than that for optimum production.

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