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Beyond the physiology of reproduction, estrogen controls the homeostasis of several tissues. Although macrophages play a key role in tissue remodeling, the interplay with estrogen is still ill defined. Using a transcriptomic approach we first obtained a comprehensive list of genes that are differentially expressed in peritoneal macrophages in response to physiological levels of 17β-estradiol (E 2 ) injected in intact female mice. Our data also showed the dynamic nature of the macrophage response to E 2  and pointed to specific biological programs induced by the hormone, with cell proliferation, immune response and wound healing being the most prominent functional categories. Indeed, the exogenous administration of E 2  and, more importantly, the endogenous hormonal surge proved to support macrophage proliferation  in vivo , as shown by cell cycle gene expression, BrdU incorporation and cell number. Furthermore, E 2  promoted an anti-inflammatory and pro-resolving macrophage phenotype, which converged on the induction of genes related to macrophage alternative activation and on IL-10 expression  in vivo . Hormone action was maintained in an experimental model of peritoneal inflammation based on zymosan injection. These findings highlight a direct effect of estrogen on macrophage expansion and phenotypic adaptation in homeostatic conditions and suggest a role for this interplay in inflammatory pathologies.

Self-renewal and phenotypic conversion are the main physiological responses of macrophages to the endogenous estrogen surge