Characterization of estrogen-responsive epithelial cell lines and their infectivity by genital Chlamydia trachomatis
Chlamydial attachment and infectivity in vitro and ascending disease and sequelae in vivo have been reported to be enhanced/modulated by estrogen. Endometrial carcinoma cell lines Ishikawa and HEC-1B and the breast cancer lines MCF-7 and HCC-1806 were examined for Chlamydia trachomatis E infectivity...
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Published in | Microbes and infection Vol. 7; no. 15; pp. 1469 - 1481 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Lausanne
Elsevier SAS
01.12.2005
Amsterdam Elsevier Paris |
Subjects | |
Online Access | Get full text |
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Summary: | Chlamydial attachment and infectivity in vitro and ascending disease and sequelae in vivo have been reported to be enhanced/modulated by estrogen.
Endometrial carcinoma cell lines Ishikawa and HEC-1B and the breast cancer lines MCF-7 and HCC-1806 were examined for
Chlamydia trachomatis E infectivity. Estrogen receptor (ER) presence was confirmed by Western blot and qRT-PCR analyses. FACS analysis was used to determine the percent of plasma membrane-localized ERs (mERs), and their activity was tested by estrogen binding and competitive estrogen antagonists assays. Chlamydiae grew in all cell lines with HEC (90%) >> MCF-7 (57%)
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Ishikawa (51%) >> HCC-1806 (20%). The cell line ER isoform composition was re-defined as: ERα + ERβ + for MCF-7, HCC-1806 and Ishikawa; and ERβ only for HEC-1B. HeLa cells were also tested and found to express ERβ, but not ERα. A small percentage of both ERs were surface-exposed and functionally active. The endometrium-predominant ERβ isoform was found in all cell lines, including those most representative of the common sites of
C. trachomatis infection. Thus, the role of chlamydial attachment/infectivity will now be analyzed in ERβ
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and—isogenic HEC-1B cells. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1286-4579 1769-714X |
DOI: | 10.1016/j.micinf.2005.05.004 |