Abstract

The mechanisms that sustain endometrial tissues at ectopic sites in patients with endometriosis are poorly understood. It is well established now that endometriosis is associated with changes in population and functions of various leukocytes, including macrophages. Macrophages are the most abundant cells found in the peritoneal fluid and are the consistent feature of endometriotic lesion. They infiltrate endometriotic lesions where they undergo alternative activation as a consequence of signals generated within the invaded tissue. However, instead of clearing endometrial cells from the peritoneal cavity and restoring local homeostasis, macrophages appear to enhance their survival and proliferation by secreting growth, remodelling and inflammatory factors which could contribute to the development of endometriosis as well as to the disease-associated chronic pelvic inflammation and symptoms. Thus, unveiling the molecular mechanisms that underlie macrophage dysfunctions is a critical area of research, which would lead to the development of novel medical treatments for endometriosis. In this chapter, we described how macrophages can play a critical role in the pathophysiology of endometriosis not only via their weakened phagocytic functions but also via other major mechanisms revealed to date.

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