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

Ali Akoum, Christine Lawson, C Lawson, Catherine Herrmann-Lavoie, C Herrmann-Lavoie, Rodolphe Maheux, R Maheux
Human Reproduction · 2007 · vol. 22(5) , pp. 1464–1473 · doi:10.1093/humrep/dem021 · PMID:17324958 · W2006143607
article OA: bronze CC0 ⤵ 29 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-06 ⓘ

Endometriosis tissues exhibit an imbalance in IL1 receptor expression, with decreased IL1R2 and increased IL1R1, which may enhance endometrial cell responsiveness to IL1 and promote lesion development.

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Abstract

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.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Receptors, Interleukin-1 Type I Receptors, Interleukin-1 Type II Adult Blotting, Western Chemokine CCL2 Chemokine CCL2 Down-Regulation Endometriosis Endometrium Endometrium Female Fluorescent Antibody Technique Humans Interleukin-1beta Interleukin-1beta Receptors, Interleukin-1 Type I Receptors, Interleukin-1 Type II Transfection Up-Regulation

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Cited by (29)

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