Localization in tissues and secretion of eotaxin by cells from normal endometrium and endometriosis

Citation
D. Hornung et al., Localization in tissues and secretion of eotaxin by cells from normal endometrium and endometriosis, J CLIN END, 85(7), 2000, pp. 2604-2608
Citations number
25
Categorie Soggetti
Endocrynology, Metabolism & Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM
ISSN journal
0021972X → ACNP
Volume
85
Issue
7
Year of publication
2000
Pages
2604 - 2608
Database
ISI
SICI code
0021-972X(200007)85:7<2604:LITASO>2.0.ZU;2-P
Abstract
Our laboratories have focused recently on the production and localization o f eotaxin, a C-C-chemokine of 8.4 kDa, whose major biological activity is t he chemoattraction of eosinophils. Given evidence of autoimmune activity in the endometriosis syndrome, we hypothesized that eosinophil chemoattractan ts might be expressed in endometriosis. In histological sections, we observ ed eotaxin protein localized mainly in epithelial cells, with only very fai nt immunostaining in the surrounding stromal cells. Prominent eotaxin accum ulation was noted in the luminal epithelium of secretory endometrium. Eotax in distribution in endometriosis was similar to that seen in eutopic endome trium but with higher levels of eotaxin staining in the glandular epitheliu m. Peritoneal fluid concentrations of eotaxin were significantly higher in women with moderate or severe endometriosis than in women with minimal or m ild endometriosis or no disease. The treatment of isolated human endometrio sis epithelial cells with estradiol, medroxyprogesterone acetate, tumor nec rosis factor-a, and interferon-gamma stimulated measurable eotaxin secretio n into the conditioned media. The results indicate that eotaxin is produced in epithelial cells of normal endometrium and endometriosis tissues, varie s across the menstrual cycle, and is elevated in women with endometriosis. We postulate that eotaxin, interacting with other known cytokines and immun e cells, contributes to an inflammatory reproductive tract environment, lea ding to endometrial or blastocyst dysfunction.