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Hum. Reprod. Advance Access originally published online on January 29, 2004
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Human Reproduction, Vol. 19, No. 3, 709-714, March 2004
© 2004 European Society of Human Reproduction and Embryology

Role of IL-18 in pathogenesis of endometriosis

H. Oku1, Y. Tsuji1,4, S.-I. Kashiwamura2, S. Adachi1, A. Kubota3, H. Okamura2 and K. Koyama1

1 Department of Obstetrics and Gynecology, 2 Laboratory of Host Defense, Institute for Advanced Medical Sciences and 3 Department of Surgical Pathology, Hyogo College of Medicine, Nishinomiya, Hyogo 663-8501, Japan

4 To whom correspondence should be addressed. e-mail: yoshi416{at}hyo-med.ac.jp

BACKGROUND: Endometriosis is a complex disease associated with a wide range of immune responses, including pain, adhesion, exudation of peritoneal fluid, elevation of cytokine levels and generation of autoantibodies. Interleukin (IL)-18 is a strong pleiotropic cytokine known to be involved in various immune diseases. The aim of this study is to elucidate the role of IL-18 in the pathogenesis of endometriosis. METHODS: IL-18 and IL-1{beta} concentrations were measured in the peritoneal fluid and sera of 39 endometriosis patients and 15 control women. Expression of IL-18 and IL-18 receptor {alpha}-chain (IL-18R{alpha}) was analysed in endometriotic tissues immunohistochemically. The effects of IL-18 on cyclooxygenase (COX)-II gene expression were analysed in peritoneal fluid monocytes and endometriotic cells of endometriosis patients. RESULTS: IL-18 concentrations in the peritoneal fluid of endometriosis patients averaged 592.57 ± 108.27 pg/ml, significantly higher than 260.50 ± 55.88 pg/ml in non-endometriotic samples. IL-18 concentrations in the serum did not differ significantly between endometriosis and control patients. Similarly, no significant differences were observed in IL-1{beta} concentrations in either the peritoneal fluid or the serum. IL-18 and IL-18R{alpha} were expressed in endometriotic tissues. IL-18R{alpha} expression was also observed in cells infiltrating into the inflammatory area of the endometriosis patients. COX-II was induced in peritoneal fluid monocytes and in endometriotic cells in response to IL-18 stimulation. CONCLUSIONS: The elevation of IL-18 in the peritoneal fluid of endometriosis patients and the induction of COX-II in peritoneal monocytes by IL-18 suggest that IL-18 plays a pathogenic role in endometriosis.

Key words: COX-II/cytokine/endometriosis/IL-18/IL-1{beta}


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