During inflammation, proinflammatory macrophages sequester iron as a well known bacteriostatic mechanism. Alternative activation of macrophages is linked to tissue repair, and during this process the expression pattern of genes important for iron homeostasis is distinct from that in proinflammatory macrophages. This leads to an increased capacity of the alternatively activated macrophages for heme uptake, via scavenger receptors, and for production of anti-inflammatory mediators via heme-oxygenase-dependent heme catabolism. Alternatively activated macrophages also release non-heme iron into tissues via ferroportin. Here, we propose that the iron-release-associated phenotype of alternatively activated macrophages significantly contributes to their role in various conditions, including tissue repair and tumor growth.
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