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Endometriosis is a gynecological disease that affects 1 in 10 women worldwide and is characterized by the presence of lesions made up of endometrial cells (ECs) outside of the uterus. Symptoms associated with endometriosis include pain and infertility. It was realized in early last century that endometriosis is an inflammatory disease. Search for the mediators of this inflammation had been one of the key areas of research in understanding the etiology of this disease. Pioneering work by Halme, Olive, and Arici’s groups provided evidences for an inflammatory peritoneal milieu and the role for macrophages in endometriosis (1-3). Publications as early as in the 1980s showed that the peritoneal macrophages are present at higher levels in women with endometriosis-associated infertility when compared to infertile women due to causes other than endometriosis or normal women (4). Just a few years later, Badawy  et al . also examined the peritoneal fluid (PF) of women with endometriosis and those who were infertile and showed that macrophages and lymphocytes were the dominant cells in their fluid. They also noted that prostaglandins, PGF2α, and PGE2 were also increased in the fluid (5).

Current assessment of the (dys)function of macrophages in endometriosis and its associated pain