Abstract: Macrophages are intimately involved in the pathophysiology of endometriosis, a chronic inflammatory disorder characterized by the growth of endometrial-like tissue (lesions) outside the uterus. By combining genetic and pharmacological macrophage depletion strategies we determined the ontogeny and function of macrophages in a mouse model of induced endometriosis. We demonstrate that lesion-resident macrophages are derived from eutopic endometrial tissue, infiltrating large peritoneal macrophages (LpM) and monocytes. Endometriosis triggers continuous recruitment of monocytes that seemingly contribute to LpM and small peritoneal macrophage (SpM) pools. Depletion of eutopic endometrial macrophages results in smaller endometriosis lesions. Constitutive inhibition of monocyte recruitment significantly reduces peritoneal macrophage populations and increases the number of lesions that develop. We propose a putative model whereby endometrial macrophages and monocyte-derived macrophages, possibly in LpM form, are ‘anti-endometriosis’. These observations highlight the importance of monocyte-derived macrophages in limiting disease progression.

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