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

被引:61
作者
Hornung, D
Dohrn, K
Sotlar, K
Greb, RR
Wallwiener, D
Kiesel, L
Taylor, RN
机构
[1] Univ Calif San Francisco, Dept Obstet Gynecol & Reprod Sci, Ctr Reprod Sci, San Francisco, CA 94143 USA
[2] Univ Tubingen, Dept Obstet & Gynecol, D-72074 Tubingen, Germany
[3] Univ Tubingen, Dept Pathol, D-72074 Tubingen, Germany
关键词
D O I
10.1210/jc.85.7.2604
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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-a, 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.
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收藏
页码:2604 / 2608
页数:5
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