Involvement of intraperitoneal macrophages and other immune cells in the pathogenesis of endometriosis

Abstract

Endometriosis is characterized by the implantation and growth of endometriotic tissues outside the uterus causing chronic pain and infertility in women of reproductive age. It is widely accepted the theory that endometriosis is caused by the implantation of endometrial tissue from retrograde menstruation; however, retrograde menstruation occurs in almost all women and other factors are required for the establishment of endometriosis. Various studies have indicated that abnormalities in the local immune environment cause the pathological development of endometriosis, and endometriosis is considered to be a chronic inflammatory disease. Focusing on the involvement of macrophages in the pathogenesis of endometriosis, we examined macrophage dysfunction in patients with endometriosis and how this dysfunction came to be. mRNA microarray analysis reveals that endometriosis macrophages have properties involved in disease progression. The intraperitoneal macrophages of patients with endometriosis have decreased antigen-presenting ability (HLA-DR) and decreased Th1 cell migration ability (CXCL10, CCL5). On the other hand, neutrophil migration (CXCL2, CXCL3), angiogenesis (IL-8, VEGF), and proinflammatory effects (IL-6, TNFα) are strong. These features of peritoneal macrophages may contribute to the pathogenesis of endometriosis.