The remedial effect of soluble interleukin-1 receptor type II on endometriosis in the nude mouse model

Liying Gao,Liang Sun,Yugui Cui,Zhen Hou,Li Gao,Jing Zhou,Yundong Mao,Suping Han,Jiayin Liu

doi:10.1016/s1674-8301(10)60007-3

Abstract

Objective Recent studies have shown that the local expression of soluble interleukin (IL) −1 receptor type II (sIL-1 RII) in endometrial tissue of women with endometriosis is decreased, and the depression of IL-1 RII was more significant in infertile women than that in fertile women with endometriosis. In this research, we investigated the remedial effect of sIL-1-RII administration on endometriosis in the nude mouse model. Methods Nineteen nude model mice with endometriosis were randomly divided into three groups: group A was treated by intraperitoneal administration with only sIL-1 RII for two weeks, group B was similarly treated with only IL-1, and group C (control) was administered saline. After 2 weeks, the size of the ectopic endometrial lesions was calculated, and the expression of vascular endothelial growth factor (VEGF) and B-cell lymphoma leukemia-2 (Bcl-2) were detected by immunohistochemistry. The IL-8 and VEGF levels in the peritoneal fluid (PF) and serum were also measured by enzyme-linked immunosorbent assay (ELISA). Results The mean size of ectopic endometrial lesion did not differ between the three groups (P > 0.05). Compared with the control, the expression of VEGF and Bcl-2 was significantly lower in group A, and higher in group B. In the three groups, the levels of IL-8 in the PF and serum were highest in group A, and lowest in group B. Conclusion sIL-1 RII may suppresse hyperplasia of ectopic endometriosis, perhaps by reducing the expression of certain cytokines, such as VEGF, IL-8, and Bcl-2, which could provide a new clinical strategy for the treatment of endometriosis.

Highlights

Endometriosis is a common gynecological disorder that affects 10%-15% of women of reproductive age and up to 50% of infertile patients
We showed that overexpression of recombinant adenovirus IL-1 RII (rAd-RII) could suppress Bcl-2 expression in ectopic endometrium, suggesting that IL-1 RII may promote apoptosis of endometriotic stromal cells through inhibition of B-cell lymphoma leukemia-2 (Bcl-2) expression
It has been demonstrated that the expression of IL1ß by peritoneal macrophages was elevated during the initial stages of endometriosis but the IL-1 receptor antagonist (IL-1ra) was usually elevated during the late stages of the disease[15]

Summary

Introduction

Endometriosis is a common gynecological disorder that affects 10%-15% of women of reproductive age and up to 50% of infertile patients. It is characterized by pelvic pain, dyspareunia and infertility as a result of the dystopic location of endometrial cells in tissues other than the uterine cavity[1]. The origin of endometriotic cells remains elusive and the most widely accepted theory on the aetiology of endometriosis is retrograde menstruation[2]. This phenomenon has been described in healthy women and can be viewed as a physiological process[3,4]. Several lines of evidence indicate that the cytokines in the peritoneal fluid (PF) of women

Methods

Results

Conclusion