Document Detail


Localization in tissues and secretion of eotaxin by cells from normal endometrium and endometriosis.
MedLine Citation:
PMID:  10902814     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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:
D Hornung; K Dohrn; K Sotlar; R R Greb; D Wallwiener; L Kiesel; R N Taylor
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of clinical endocrinology and metabolism     Volume:  85     ISSN:  0021-972X     ISO Abbreviation:  J. Clin. Endocrinol. Metab.     Publication Date:  2000 Jul 
Date Detail:
Created Date:  2000-08-08     Completed Date:  2000-08-08     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0375362     Medline TA:  J Clin Endocrinol Metab     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  2604-8     Citation Subset:  AIM; IM    
Affiliation:
Department of Obstetrics and Gynecology, University of Tübingen, Germany.
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MeSH Terms
Descriptor/Qualifier:
Adult
Ascitic Fluid / chemistry,  metabolism
Case-Control Studies
Cells, Cultured
Chemokine CCL11
Chemokines, CC*
Chemotactic Factors, Eosinophil / chemistry,  metabolism*
Cytokines / chemistry,  metabolism*,  pharmacology
Endometriosis / metabolism*,  pathology
Endometrium / cytology,  metabolism*
Enzyme-Linked Immunosorbent Assay
Estradiol / pharmacology
Female
Humans
Immunohistochemistry
Interferon-gamma / pharmacology
Medroxyprogesterone / pharmacology
Progesterone Congeners / pharmacology
Tumor Necrosis Factor-alpha / pharmacology
Grant Support
ID/Acronym/Agency:
U54-HD-37321/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/CCL11 protein, human; 0/Chemokine CCL11; 0/Chemokines, CC; 0/Chemotactic Factors, Eosinophil; 0/Cytokines; 0/Progesterone Congeners; 0/Tumor Necrosis Factor-alpha; 50-28-2/Estradiol; 520-85-4/Medroxyprogesterone; 82115-62-6/Interferon-gamma

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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