Role of Interleukin-6 and Its Receptor in Endometriosis
Shihui Li1, Xiaoxia Fu1, Tingting Wu1
1Department of Obstetrics and Gynecology, Women's Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China (mainland).
Abstract:
BACKGROUND Studies have shown that the concentration of interleukin (IL)-6 in peritoneal fluid is increased in patients with endometriosis; however, whether the disorders involving IL-6 contribute to the development of endometriosis is still unclear. In the present study, we evaluated the potential role of IL-6 and IL-6 receptor (IL-6R) in the pathogenesis of endometriosis. MATERIAL AND METHODS We examined activated macrophages and the expression of membrane-binding receptor (mIL-6R) in peritoneal fluid using flow cytometry. The levels of IL-6 and the IL-6 soluble receptor (sIL-6R) in peritoneal fluid and plasma in patients with endometriosis was measured by an enzyme-linked immunosorbent assay. RESULTS Activated macrophages and mIL-6R in peritoneal fluid were increased in patients with endometriosis. IL-6 and sIL-6R in peritoneal fluid were also increased in patients with endometriosis; however, there was an increase in plasma IL-6 and a decrease in plasma sIL-6R. The endometriosis group was categorized into 2 groups according to the retrospective American Fertility Society Score (r-AFS): group A and group B. Peritoneal fluid sIL-6R in endometriosis group B was significantly higher than in endometriosis group A and the control group. CONCLUSIONS Disorders involving IL-6 and IL-6R are correlated with the etiology of endometriosis. An increase in sIL-6R in peritoneal fluid promotes the development of endometriosis by enhancing the bioactivity of IL-6.
Related Concept Videos
T Cell Types and Functions
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Receptor Downregulation in MVBs
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...
Oogenesis


