title: Localization in tissues and secretion of eotaxin by cells from normal endometrium and endometriosis.
abstract: Our laboratories have focused recently on the production and localization of eotaxin, a C-C-chemokine of 8.4 kDa, whose major biological activity is the chemoattraction of eosinophils. Given evidence of autoimmune activity in the endometriosis syndrome, we hypothesized that eosinophil chemoattractants might be expressed in endometriosis. In histological sections, we observed eotaxin protein localized mainly in epithelial cells, with only very faint immunostaining in the surrounding stromal cells. Prominent eotaxin accumulation was noted in the luminal epithelium of secretory endometrium. Eotaxin distribution in endometriosis was similar to that seen in eutopic endometrium but with higher levels of eotaxin staining in the glandular epithelium. Peritoneal fluid concentrations of eotaxin were significantly higher in women with moderate or severe endometriosis than in women with minimal or mild endometriosis or no disease. The treatment of isolated human endometriosis epithelial cells with estradiol, medroxyprogesterone acetate, tumor necrosis factor-alpha, and interferon-gamma stimulated measurable eotaxin secretion into the conditioned media. The results indicate that eotaxin is produced in epithelial cells of normal endometrium and endometriosis tissues, varies across the menstrual cycle, and is elevated in women with endometriosis. We postulate that eotaxin, interacting with other known cytokines and immune cells, contributes to an inflammatory reproductive tract environment, leading to endometrial or blastocyst dysfunction.
authors.affiliation: Department of Obstetrics and Gynecology, University of Tübingen, Germany.
authors.forename: D
authors.initials: D
authors.lastname: Hornung
authors.forename: K
authors.initials: K
authors.lastname: Dohrn
authors.forename: K
authors.initials: K
authors.lastname: Sotlar
authors.forename: R R
authors.initials: RR
authors.lastname: Greb
authors.forename: D
authors.initials: D
authors.lastname: Wallwiener
authors.forename: L
authors.initials: L
authors.lastname: Kiesel
authors.forename: R N
authors.initials: RN
authors.lastname: Taylor
mesh_terms: D000328:Adult; D001202:Ascitic Fluid / Q000737:chemistry / Q000378:metabolism; D016022:Case-Control Studies; D002478:Cells, Cultured; D054413:Chemokine CCL11; D019742:Chemokines, CC; D002631:Chemotactic Factors, Eosinophil / Q000737:chemistry / Q000378:metabolism*; D016207:Cytokines / Q000737:chemistry / Q000378:metabolism* / Q000494:pharmacology; D004715:Endometriosis / Q000378:metabolism* / Q000473:pathology; D004717:Endometrium / Q000166:cytology / Q000378:metabolism*; D004797:Enzyme-Linked Immunosorbent Assay; D004958:Estradiol / Q000494:pharmacology; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007371:Interferon-gamma / Q000494:pharmacology; D008525:Medroxyprogesterone / Q000494:pharmacology; D045167:Progesterone Congeners / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: C515456:CCL11 protein, human; D054413:Chemokine CCL11; D019742:Chemokines, CC; D002631:Chemotactic Factors, Eosinophil; D016207:Cytokines; D045167:Progesterone Congeners; D014409:Tumor Necrosis Factor-alpha; D004958:Estradiol; D007371:Interferon-gamma; D008525:Medroxyprogesterone