The multifaceted role of oestrogen in enhancing Chlamydia trachomatis infection in polarized human endometrial epithelial cells.
Identifieur interne : 002420 ( Main/Exploration ); précédent : 002419; suivant : 002421The multifaceted role of oestrogen in enhancing Chlamydia trachomatis infection in polarized human endometrial epithelial cells.
Auteurs : Jennifer Vanover Hall [États-Unis] ; Maria Schell ; Sophie Dessus-Babus ; Cheryl G. Moore ; Judy D. Whittimore ; Melanie Sal ; Brian D. Dill ; Priscilla B. WyrickSource :
- Cellular microbiology [ 1462-5822 ] ; 2011.
Descripteurs français
- KwdFr :
- Analyse de profil d'expression de gènes, Cellules épithéliales (), Cellules épithéliales (microbiologie), Chlamydia trachomatis (croissance et développement), Chlamydia trachomatis (pathogénicité), Humains, Infections à Chlamydia (microbiologie), Lignée cellulaire, Microscopie électronique à transmission, Modèles biologiques, Oestrogènes (métabolisme), Récepteurs des oestrogènes (métabolisme), Techniques de coculture.
- MESH :
- croissance et développement : Chlamydia trachomatis.
- microbiologie : Cellules épithéliales, Infections à Chlamydia.
- métabolisme : Oestrogènes, Récepteurs des oestrogènes.
- pathogénicité : Chlamydia trachomatis.
- Analyse de profil d'expression de gènes, Cellules épithéliales, Humains, Lignée cellulaire, Microscopie électronique à transmission, Modèles biologiques, Techniques de coculture.
English descriptors
- KwdEn :
- Cell Line, Chlamydia Infections (microbiology), Chlamydia trachomatis (growth & development), Chlamydia trachomatis (pathogenicity), Coculture Techniques, Epithelial Cells (drug effects), Epithelial Cells (microbiology), Estrogens (metabolism), Gene Expression Profiling, Humans, Microscopy, Electron, Transmission, Models, Biological, Receptors, Estrogen (metabolism).
- MESH :
- chemical , metabolism : Estrogens, Receptors, Estrogen.
- drug effects : Epithelial Cells.
- growth & development : Chlamydia trachomatis.
- microbiology : Chlamydia Infections, Epithelial Cells.
- pathogenicity : Chlamydia trachomatis.
- Cell Line, Coculture Techniques, Gene Expression Profiling, Humans, Microscopy, Electron, Transmission, Models, Biological.
Abstract
The oestrogen receptor (ER) α-β+ HEC-1B and the ERα+β+ Ishikawa (IK) cell lines were investigated to dissect the effects of oestrogen exposure on several parameters of Chlamydia trachomatis infection. Antibody blockage of ERα or ERβ alone or simultaneously significantly decreased C. trachomatis infectivity (45-68%). Addition of the ERβ antagonist, tamoxifen, to IK or HEC-1B prior to or after chlamydial infection caused a 30-90% decrease in infectivity, the latter due to disrupted eukaryotic organelles. In vivo, endometrial glandular epithelial cells are stimulated by hormonally influenced stromal signals. Accordingly, chlamydial infectivity was significantly increased by 27% and 21% in IK and HEC-1B cells co-cultured with SHT-290 stromal cells exposed to oestrogen. Endometrial stromal cell/epithelial cell co-culture revealed indirect effects of oestrogen on phosphorylation of extracellular signal-regulated kinase and calcium-dependant phospholipase A2 and significantly increased production of interleukin (IL)-8 and IL-6 in both uninfected and chlamydiae-infected epithelial cells. These results indicate that oestrogen and its receptors play multiple roles in chlamydial infection: (i) membrane oestrogen receptors (mERs) aid in chlamydial entry into host cells, and (ii) mER signalling may contribute to inclusion development during infection. Additionally, enhancement of chlamydial infection is affected by hormonally influenced stromal signals in conjunction with direct oestrogen stimulation of the human epithelia.
DOI: 10.1111/j.1462-5822.2011.01608.x
PubMed: 21615662
Affiliations:
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Whittimore</name></author><author><name sortKey="Sal, Melanie" sort="Sal, Melanie" uniqKey="Sal M" first="Melanie" last="Sal">Melanie Sal</name></author><author><name sortKey="Dill, Brian D" sort="Dill, Brian D" uniqKey="Dill B" first="Brian D" last="Dill">Brian D. Dill</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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Antibody blockage of ERα or ERβ alone or simultaneously significantly decreased C. trachomatis infectivity (45-68%). Addition of the ERβ antagonist, tamoxifen, to IK or HEC-1B prior to or after chlamydial infection caused a 30-90% decrease in infectivity, the latter due to disrupted eukaryotic organelles. In vivo, endometrial glandular epithelial cells are stimulated by hormonally influenced stromal signals. Accordingly, chlamydial infectivity was significantly increased by 27% and 21% in IK and HEC-1B cells co-cultured with SHT-290 stromal cells exposed to oestrogen. Endometrial stromal cell/epithelial cell co-culture revealed indirect effects of oestrogen on phosphorylation of extracellular signal-regulated kinase and calcium-dependant phospholipase A2 and significantly increased production of interleukin (IL)-8 and IL-6 in both uninfected and chlamydiae-infected epithelial cells. These results indicate that oestrogen and its receptors play multiple roles in chlamydial infection: (i) membrane oestrogen receptors (mERs) aid in chlamydial entry into host cells, and (ii) mER signalling may contribute to inclusion development during infection. Additionally, enhancement of chlamydial infection is affected by hormonally influenced stromal signals in conjunction with direct oestrogen stimulation of the human epithelia.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Tennessee</li></region></list><tree><noCountry><name sortKey="Dessus Babus, Sophie" sort="Dessus Babus, Sophie" uniqKey="Dessus Babus S" first="Sophie" last="Dessus-Babus">Sophie Dessus-Babus</name><name sortKey="Dill, Brian D" sort="Dill, Brian D" uniqKey="Dill B" first="Brian D" last="Dill">Brian D. Dill</name><name sortKey="Moore, Cheryl G" sort="Moore, Cheryl G" uniqKey="Moore C" first="Cheryl G" last="Moore">Cheryl G. Moore</name><name sortKey="Sal, Melanie" sort="Sal, Melanie" uniqKey="Sal M" first="Melanie" last="Sal">Melanie Sal</name><name sortKey="Schell, Maria" sort="Schell, Maria" uniqKey="Schell M" first="Maria" last="Schell">Maria Schell</name><name sortKey="Whittimore, Judy D" sort="Whittimore, Judy D" uniqKey="Whittimore J" first="Judy D" last="Whittimore">Judy D. Whittimore</name><name sortKey="Wyrick, Priscilla B" sort="Wyrick, Priscilla B" uniqKey="Wyrick P" first="Priscilla B" last="Wyrick">Priscilla B. Wyrick</name></noCountry><country name="États-Unis"><region name="Tennessee"><name sortKey="Hall, Jennifer Vanover" sort="Hall, Jennifer Vanover" uniqKey="Hall J" first="Jennifer Vanover" last="Hall">Jennifer Vanover Hall</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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