Educational Lecture 1 - Role of Innate and Adaptive Immunity in Endometriosis

Abstract

Endometriosis is a multifactorial disease that mainly affects women of reproductive age and is associated with chronic pelvic pain and infertility. The exact pathogenesis of this disease is still debatable. In 2010, we established “bacterial contamination hypothesis”, a new concept in endometriosis. As a component of innate immunity, the role of bacterial endotoxin (lipopolysaccharide, LPS) and Toll-like receptor 4 (TLR4) in endometriosis was investigated and the possible source of endotoxin in uterine and pelvic environment was examined. We found that LPS regulates the pro-inflammatory response in pelvis and growth of endometriosis via LPS/TLR4 cascade. The highly contaminated menstrual blood with Escherichia coli was associated with significantly higher levels of endotoxin in the menstrual fluid and peritoneal fluid collected from women with endometriosis than that in control women. Most recently we examined the hypothesis that antibiotic treatment with or without GnRHa may decrease IUMC with reduction of inflammation and cell growth in women with endometriosis. We will report our current findings on this issue. The innate immunity and adaptive immunity are integral part of immune system. As a component of adaptive immunity, regulatory T (Treg) cells and T-helper-17 (Th17) cells may be involved in endometriosis. A reciprocal balance between Treg and Th17 cells may promote or retard the growth of endometriosis. Our knowledge on the changes in the percentages of Treg and Th-17 cells in the peripheral blood and in the peritoneal fluid of women with early and advanced endometriosis in unclear. We will report our current findings on this issue.