Expression of intercellular adhesion molecule (ICAM)-1 mRNA and protein isenhanced in endometriosis versus endometrial stromal cells in culture

The relationship between the immune and the endometrial systems has been re cently suggested to be critical to the development of endometriosis. We pre viously showed that one of the molecules involved in the complex events tha t allow this interaction is the adhesion molecule intercellular adhesion mo lecule (ICAM)-1. This study was designed to evaluate whether differences in ICAM-1 mRNA and protein expression might exist between eutopic endometrial cells and ectopic cells derived from endometriomas. Stromal cells were dis persed from samples of endometrium and ovarian endometriomas biopsied synch ronously from 24 patients with endometriosis. We established that the relat ive expression of ICAM transcript was significantly higher in ectopic cells than that found in cultures derived from endometrial samples. Moreover, ec topic cells demonstrated a significant overexpression of ICAM-1 protein in both its cell-bound and soluble form (sICAM-1) (P < 0.05). Interestingly, e ndometrial secretion of sICAM-1 was shown to vary during the menstrual cycl e as proliferative phase samples released significantly higher concentratio ns of the soluble protein compared to the secretory phase. In contrast, thi s cycle-dependent pattern was absent in stromal cells derived from endometr iomas. Moreover, interleukin (IL-1 beta) was able to increase sICAM-1 shedd ing from endometrial cells in a concentration-dependent manner and this IL- 1 beta-mediated induction could be slightly enhanced by oestradiol. As sICA M-1 is able to interfere with ICAM-1-mediated immune functions, the release of higher concentrations from ectopic samples may be the mechanism by whic h ectopic endometrial cells escape immunosurveillance.