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Hum. Reprod. Advance Access originally published online on February 26, 2007
Human Reproduction 2007 22(5):1464-1473; doi:10.1093/humrep/dem021
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© The Author 2007. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Imbalance in the expression of the activating type I and the inhibitory type II interleukin 1 receptors in endometriosis

Ali Akoum1,2,3, C. Lawson1,2, C. Herrmann-Lavoie1,2 and R. Maheux1,2

1 Unité d'Endocrinologie de la Reproduction, Centre de Recherche, Hôpital Saint-François d'Assise, Centre Hospitalier Universitaire de Québec, Canada 2 Département d'Obstétrique et Gynécologie, Faculté de Médecine, Université Laval, Québec, Canada

3 To whom correspondence should be addressed at: Unité d'Endocrinologie de la Reproduction, Centre de Recherche, Hôpital Saint-François d'Assise, Centre Hospitalier Universitaire de Québec, 10 rue de l'Espinay, Local D0-711, Québec, Canada G1L 3L5. Tel: +1 418 525 4444 53329; Fax: +1 418 525 4195; E-mail: ali.akoum{at}crsfa.ulaval.ca

BACKGROUND: The ectopic establishment and progression of endometrial tissue is dependent upon its interaction with and responsiveness to the stimuli present in its new environment. Immune cell-derived cytokines, such as interleukin 1 (IL1), may alone or in concert with estrogens enhance the capability of ectopic endometrial cells to implant and develop into the host tissue. The objective of this study was to further evaluate the expression and significance of IL1 receptor type I (IL1R1), the signalling receptor that mediates cell activation by IL1, and IL1 receptor type II (IL1R2), a potent and specific down-regulator of IL1 action, in normal compared to endometriotic/endometrial tissues.

METHODS: Techniques included immunohistochemistry, immunofluorescent staining, ELISA, western blotting and endometriotic cell culture transfection.

RESULTS: Our study showed an imbalance in the expression of IL1R1 and IL1R2 in eutopic, and particularly in ectopic, endometrial tissues of women with endometriosis. Actually, a decreased IL1R2 expression is predominant in the eutopic and ectopic endometrium of women with endometriosis when compared with normal women, whereas a concomitant increase in IL1R1 expression occurs in ectopic endometrial tissue in comparison to eutopic endometrial tissue of normal or endometriotic women, particularly in the initial and most active implants. Transfection of endometriotic cells with a cDNA coding for IL1R2 resulted in a significant decrease in IL1-induced secretion of vascular endothelial cell growth factor and monocyte chemotactic protein 1.

CONCLUSIONS: IL1R1/IL1R2 imbalance may amplify endometrial cell responsiveness to IL1 and represent a key mechanism underlying the ability of these cells to implant and develop into host tissues.

Key words: endometriosis/endometrium/IL1R1/IL1R2/lesion

Submitted on December 18, 2006; resubmitted on January 10, 2007; accepted on January 15, 2007.


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