title: Imbalance in the expression of the activating type I and the inhibitory type II interleukin 1 receptors in endometriosis.
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.
authors.affiliation: Unité d'Endocrinologie de la Reproduction, Centre de Recherche, Hôpital Saint-François d'Assise, Centre Hospitalier Universitaire de Québec, Canada. ali.akoum@crsfa.ulaval.ca
authors.forename: Ali
authors.initials: A
authors.lastname: Akoum
authors.forename: C
authors.initials: C
authors.lastname: Lawson
authors.forename: C
authors.initials: C
authors.lastname: Herrmann-Lavoie
authors.forename: R
authors.initials: R
authors.lastname: Maheux
mesh_terms: D000328:Adult; D015153:Blotting, Western; D018932:Chemokine CCL2 / Q000096:biosynthesis; D015536:Down-Regulation; D004715:Endometriosis / Q000503:physiopathology*; D004717:Endometrium / Q000378:metabolism; D005260:Female; D005455:Fluorescent Antibody Technique; D006801:Humans; D053583:Interleukin-1beta / Q000235:genetics; D053573:Receptors, Interleukin-1 Type I / Q000096:biosynthesis*; D053574:Receptors, Interleukin-1 Type II / Q000096:biosynthesis*; D014162:Transfection; D015854:Up-Regulation; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis
chemical_list: D018932:Chemokine CCL2; C508590:IL1R1 protein, human; C508592:IL1R2 protein, human; D053583:Interleukin-1beta; D053573:Receptors, Interleukin-1 Type I; D053574:Receptors, Interleukin-1 Type II; D042461:Vascular Endothelial Growth Factor A