Abstract: Endometriosis(EMs) is a common disease in fertile women，leading to dysmenorrhea, pelvic pain and even infertility. Recent studies have indicated that the pathogenesis of EMs is not only affected by hormones, but also associated with chronic inflammation. Toll like receptor 4 (TLR4), a kind of inflammatory mediators existing in endometrial cells, plays an important role in host innate immunity against pathogen. It may be pivotal in the occurrence and development of EMs. During menstruation, pathogens from the lower genital tract and the shed endometrial tissue fragments enter the upper genital tract with retrograde menstruation. Pathogens activate TLR signal pathway on ectopic endometrial cells, recruit and activate immune cells (e.g. macrophages etc.) to trigger local inflammatory response and promote the secretion of different inflammatory factors and growth factors, thus stimulate the proliferation of endometrial cells. The sustained inflammatory damage causes the injured cells to induce stress reaction and release other endogenous ligands (e.g. HSP70, HMGB-1, etc.), so that TLR4 signal pathway could be further activated. The joint effect of above two reactions activate the inflammatory microenvironment to promote the adhesion, invasion and proliferation of endometrial cells, and ultimately lead to the occurrence and development of EMs. This theory suggests that anti-inflammatory remedy against TLR4 signal pathway may become a new direction for treating EMs.

Key words: Endometriosis , Inflammation, Stress reaction, Toll-like receptor 4;, TLR4 signal pathway