Intercellular adhesion molecule-1 expression in human endometrium

Background: Neutrophils infiltrate the endometrium pre-menstrually and after long-term progestin only-contraceptive (LTPOC) treatment. Trafficking of neutrophils involves endothelial cell-expressed intercellular adhesion molecule (ICAM-1). Previous studies observed that ICAM-1 was immunolocalized to the endothelium of endometrial specimens across the menstrual cycle, but disagreed as to whether extra-endothelial cell types express ICAM-1 and whether ICAM-1 expression varies across the menstrual cycle. Methods: Endometrial biopsies were obtained from women across the menstrual cycle and from those on LTPOC treatment (either Mirena or Norplant). The biopsies were formalin-fixed and paraffin-embedded with subsequent immunohistochemical staining for ICAM-1. Results: The current study found prominent ICAM-1 staining in the endometrial endothelium that was of equivalent intensity in different blood vessel types irrespective of the steroidal or inflammatory endometrial milieu across the menstrual cycle and during LTPOC therapy. Unlike the endothelial cells, the glands were negative and the stromal cells were weakly positive for ICAM immunostaining. Conclusion: The results of the current study suggest that altered expression of ICAM-1 by endothelial cells does not account for the influx of neutrophils into the premenstrual and LTPOCderived endometrium. Such neutrophil infiltration may depend on altered expression of neutrophil chemoattractants. Background The premenstrual human endometrium displays increased prostaglandin-generating capacity, elevated levels of inflammatory cytokines [1,2] and a leukocyte infiltrate that comprises nearly one-half of the cell population [3-5]. Among endometrial leukocyte subtypes, neutrophils are virtually absent until the mid-luteal phase, but comprise a significant portion of the leukocytes in the Published: 30 January 2006 Reproductive Biology and Endocrinology 2006, 4:2 doi:10.1186/1477-7827-4-2 Received: 28 June 2005 Accepted: 30 January 2006 This article is available from: http://www.rbej.com/content/4/1/2 © 2006 Schatz et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Reproductive Biology and Endocrinology 2006, 4:2 http://www.rbej.com/content/4/1/2