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Characterization of estrogen-responsive epithelial cell lines and their infectivity by genital Chlamydia trachomatis.

Identifieur interne : 002F18 ( Main/Exploration ); précédent : 002F17; suivant : 002F19

Characterization of estrogen-responsive epithelial cell lines and their infectivity by genital Chlamydia trachomatis.

Auteurs : Natalia V. Guseva [États-Unis] ; Sophie C. Dessus-Babus ; Judy D. Whittimore ; Cheryl G. Moore ; Priscilla B. Wyrick

Source :

RBID : pubmed:16046168

Descripteurs français

English descriptors

Abstract

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%)>Ishikawa (51%) > HCC-1806 (20%). The cell line ER isoform composition was re-defined as: ERalpha + ERbeta + for MCF-7, HCC-1806 and Ishikawa; and ERbeta only for HEC-1B. HeLa cells were also tested and found to express ERbeta, but not ERalpha. A small percentage of both ERs were surface-exposed and functionally active. The endometrium-predominant ERbeta 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 ERbeta+and-isogenic HEC-1B cells.

DOI: 10.1016/j.micinf.2005.05.004
PubMed: 16046168


Affiliations:


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Le document en format XML

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<term>Chlamydia trachomatis (growth & development)</term>
<term>Cytoplasm (microbiology)</term>
<term>Cytoplasm (ultrastructure)</term>
<term>Epithelial Cells (microbiology)</term>
<term>Epithelial Cells (ultrastructure)</term>
<term>Estrogens (analysis)</term>
<term>Estrogens (physiology)</term>
<term>Flow Cytometry</term>
<term>Gene Expression</term>
<term>Humans</term>
<term>Inclusion Bodies (microbiology)</term>
<term>Inclusion Bodies (ultrastructure)</term>
<term>Microscopy, Confocal</term>
<term>RNA, Messenger (analysis)</term>
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<term>Receptors, Estrogen (genetics)</term>
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<term>Chlamydia trachomatis (croissance et développement)</term>
<term>Corps d'inclusion (microbiologie)</term>
<term>Corps d'inclusion (ultrastructure)</term>
<term>Cytométrie en flux</term>
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<term>Cytoplasme (ultrastructure)</term>
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<term>Lignée cellulaire</term>
<term>Membrane cellulaire ()</term>
<term>Microscopie confocale</term>
<term>Oestrogènes (analyse)</term>
<term>Oestrogènes (physiologie)</term>
<term>RT-PCR</term>
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<term>Cytométrie en flux</term>
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<term>Humains</term>
<term>Lignée cellulaire</term>
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<div type="abstract" xml:lang="en">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%)>Ishikawa (51%) > HCC-1806 (20%). The cell line ER isoform composition was re-defined as: ERalpha + ERbeta + for MCF-7, HCC-1806 and Ishikawa; and ERbeta only for HEC-1B. HeLa cells were also tested and found to express ERbeta, but not ERalpha. A small percentage of both ERs were surface-exposed and functionally active. The endometrium-predominant ERbeta 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 ERbeta+and-isogenic HEC-1B cells.</div>
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