Macrophage-Mediated Defensive Mechanisms Involving Zinc Homeostasis in Bacterial Infection

Abstract Zinc homeostasis in macrophages is essential for maintaining their antimicrobial functions, and a growing body of evidence indicates that both zinc depletion and excess zinc in myeloid cells decrease bacterial survival. In macrophages, maintaining intracellular and extracellular zinc levels via zinc transporter proteins, including Slc30a and Slc39a family members, plays an important role in the response to immunological signals and infection. Recently, studies have found that macrophages utilize a variety of zinc-modulating mechanisms, thus expanding our knowledge regarding the role that zinc plays in response to bacterial infection. Here, we review recent progress with respect to altered zinc metabolism in macrophages and the consequences with respect to fighting invading pathogens.