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Updated: Jul 15, 2026

Mouse Model of Surgically-induced Endometriosis by Auto-transplantation of Uterine Tissue
Published on: January 6, 2012
Role of interleukin-1 receptor type II in the pathogenesis of endometriosis
Zhen Hou1, Jing Zhou, Xiang Ma
1Center of Clinical Reproductive Medicine, Department of Obstetrics and Gynecology, First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Objective:
To determine the role of interleukin-1 receptor type II (IL-1RII) in the pathogenesis of endometriosis.
Design:
Cultures of endometrial cells exposed to soluble IL-1RII or the recombinant adenovirus of IL-1RII (rAd-RII).
Setting:
Gynecology clinic and human reproduction research laboratory.
Patient(S):
Women with endometriosis undergoing hysterectomy.
Intervention(S):
Cell culture media were collected 12 hours after addition of soluble IL-1RII or infection of rAd-RII.
Main Outcome Measure(S):
The levels of IL-6 and IL-8 in the culture media were measured via enzyme-linked immunoabsorbent assay. Furthermore, proteins of the cells were collected for two-dimensional electrophoresis and the differential protein expression was identified by the matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry.
Result(S):
Addition of soluble IL-1RII (2.0 microg/mL) significantly inhibited IL-1 beta-induced IL-6 and IL-8 secretion by endometrial cells in vitro. Infection of endometrial cells with rAd-RII significantly decreased IL-1 beta-induced IL-8 secretion, compared with the PBS and rAd-LacZ controls but had no significant effect on IL-6 secretion. Proteins of the infected cells were collected for two-dimensional electrophoresis, and intensities of 62 spots were significantly increased or decreased when compared with those in the PBS group. Thirty-four proteins were identified by MALDI-TOF mass spectrometry. The majority of the identified proteins are related to cellular metabolism and proliferation.
Conclusion(S):
These results suggest that IL-1RII can neutralize IL-1 beta and counteract its effect on endometrial stromal cells, and may provide a new clinical strategy for the treatment of endometriosis.
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