Characterization of estrogen-responsive epithelial cell lines and their infectivity by genital Chlamydia trachomatis.
Identifieur interne : 002322 ( PubMed/Curation ); précédent : 002321; suivant : 002323Characterization 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. WyrickSource :
- Microbes and infection [ 1286-4579 ] ; 2005.
Descripteurs français
- KwdFr :
- ARN messager (analyse), Cellules épithéliales (microbiologie), Cellules épithéliales (ultrastructure), Chlamydia trachomatis (croissance et développement), Corps d'inclusion (microbiologie), Corps d'inclusion (ultrastructure), Cytométrie en flux, Cytoplasme (microbiologie), Cytoplasme (ultrastructure), Expression des gènes, Humains, Lignée cellulaire, Membrane cellulaire (), Microscopie confocale, Oestrogènes (analyse), Oestrogènes (physiologie), RT-PCR, Récepteurs des oestrogènes (analyse), Récepteurs des oestrogènes (génétique), Technique de Western.
- MESH :
- analyse : ARN messager, Oestrogènes, Récepteurs des oestrogènes.
- croissance et développement : Chlamydia trachomatis.
- génétique : Récepteurs des oestrogènes.
- microbiologie : Cellules épithéliales, Corps d'inclusion, Cytoplasme.
- physiologie : Oestrogènes.
- Cellules épithéliales, Corps d'inclusion, Cytométrie en flux, Cytoplasme, Expression des gènes, Humains, Lignée cellulaire, Membrane cellulaire, Microscopie confocale, RT-PCR, Technique de Western.
English descriptors
- KwdEn :
- Blotting, Western, Cell Line, Cell Membrane (chemistry), Chlamydia trachomatis (growth & development), Cytoplasm (microbiology), Cytoplasm (ultrastructure), Epithelial Cells (microbiology), Epithelial Cells (ultrastructure), Estrogens (analysis), Estrogens (physiology), Flow Cytometry, Gene Expression, Humans, Inclusion Bodies (microbiology), Inclusion Bodies (ultrastructure), Microscopy, Confocal, RNA, Messenger (analysis), Receptors, Estrogen (analysis), Receptors, Estrogen (genetics), Reverse Transcriptase Polymerase Chain Reaction.
- MESH :
- chemical , analysis : Estrogens, RNA, Messenger, Receptors, Estrogen.
- chemistry : Cell Membrane.
- chemical , genetics : Receptors, Estrogen.
- growth & development : Chlamydia trachomatis.
- microbiology : Cytoplasm, Epithelial Cells, Inclusion Bodies.
- chemical , physiology : Estrogens.
- ultrastructure : Cytoplasm, Epithelial Cells, Inclusion Bodies.
- Blotting, Western, Cell Line, Flow Cytometry, Gene Expression, Humans, Microscopy, Confocal, Reverse Transcriptase Polymerase Chain Reaction.
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
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Moore</name></author><author><name sortKey="Wyrick, Priscilla B" sort="Wyrick, Priscilla B" uniqKey="Wyrick P" first="Priscilla B" last="Wyrick">Priscilla B. 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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></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16046168</PMID><DateCompleted><Year>2006</Year><Month>03</Month><Day>07</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">1286-4579</ISSN><JournalIssue CitedMedium="Print"><Volume>7</Volume><Issue>15</Issue><PubDate><Year>2005</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Microbes and infection</Title><ISOAbbreviation>Microbes Infect.</ISOAbbreviation></Journal><ArticleTitle>Characterization of estrogen-responsive epithelial cell lines and their infectivity by genital Chlamydia trachomatis.</ArticleTitle><Pagination><MedlinePgn>1469-81</MedlinePgn></Pagination><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Guseva</LastName><ForeName>Natalia V</ForeName><Initials>NV</Initials><AffiliationInfo><Affiliation>Department of Microbiology, J.H. Quillen College of Medicine, East Tennessee State University, Box 70579, VA#1-Rm. 141, Johnson City, 37614, USA. guseva@etsu.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dessus-Babus</LastName><ForeName>Sophie C</ForeName><Initials>SC</Initials></Author><Author ValidYN="Y"><LastName>Whittimore</LastName><ForeName>Judy D</ForeName><Initials>JD</Initials></Author><Author ValidYN="Y"><LastName>Moore</LastName><ForeName>Cheryl G</ForeName><Initials>CG</Initials></Author><Author ValidYN="Y"><LastName>Wyrick</LastName><ForeName>Priscilla B</ForeName><Initials>PB</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>AI13446</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2005</Year><Month>06</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>France</Country><MedlineTA>Microbes Infect</MedlineTA><NlmUniqueID>100883508</NlmUniqueID><ISSNLinking>1286-4579</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004967">Estrogens</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011960">Receptors, Estrogen</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D015153" MajorTopicYN="N">Blotting, Western</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002462" MajorTopicYN="N">Cell Membrane</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002692" MajorTopicYN="N">Chlamydia trachomatis</DescriptorName><QualifierName UI="Q000254" MajorTopicYN="Y">growth & development</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003593" MajorTopicYN="N">Cytoplasm</DescriptorName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName><QualifierName UI="Q000648" MajorTopicYN="N">ultrastructure</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004847" MajorTopicYN="N">Epithelial Cells</DescriptorName><QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName><QualifierName UI="Q000648" MajorTopicYN="N">ultrastructure</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004967" MajorTopicYN="N">Estrogens</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005434" MajorTopicYN="N">Flow Cytometry</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015870" MajorTopicYN="N">Gene Expression</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002479" MajorTopicYN="N">Inclusion Bodies</DescriptorName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName><QualifierName UI="Q000648" MajorTopicYN="N">ultrastructure</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018613" MajorTopicYN="N">Microscopy, Confocal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012333" MajorTopicYN="N">RNA, Messenger</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011960" MajorTopicYN="N">Receptors, Estrogen</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020133" MajorTopicYN="N">Reverse Transcriptase Polymerase Chain Reaction</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2005</Year><Month>05</Month><Day>04</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2005</Year><Month>05</Month><Day>06</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2005</Year><Month>7</Month><Day>28</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>3</Month><Day>8</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2005</Year><Month>7</Month><Day>28</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16046168</ArticleId><ArticleId IdType="pii">S1286-4579(05)00185-1</ArticleId><ArticleId IdType="doi">10.1016/j.micinf.2005.05.004</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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