| Neisseria gonorrhoeae infection protects human endocervical epithelial cells from apoptosis via expression of host antiapoptotic proteins. | |
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MedLine Citation:
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PMID: 19546192 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Several microbial pathogens can modulate the host apoptotic response to infection, which may contribute to immune evasion. Various studies have reported that infection with the sexually transmitted disease pathogen Neisseria gonorrhoeae can either inhibit or induce apoptosis. N. gonorrhoeae infection initiates at the mucosal epithelium, and in women, cells from the ectocervix and endocervix are among the first host cells encountered by this pathogen. In this study, we defined the antiapoptotic effect of N. gonorrhoeae infection in human endocervical epithelial cells (End/E6E7 cells). We first established that N. gonorrhoeae strain FA1090B failed to induce cell death in End/E6E7 cells. Subsequently, we demonstrated that stimulation with N. gonorrhoeae protected these cells from staurosporine (STS)-induced apoptosis. Importantly, only End/E6E7 cells incubated with live bacteria and in direct association with N. gonorrhoeae were protected from STS-induced apoptosis, while heat-killed and antibiotic-killed bacteria failed to induce protection. Stimulation of End/E6E7 cells with live N. gonorrhoeae induced NF-kappaB activation and resulted in increased gene expression of the NF-kappaB-regulated antiapoptotic genes bfl-1, cIAP-2, and c-FLIP. Furthermore, cIAP-2 protein levels also increased in End/E6E7 cells incubated with gonococci. Collectively, our results indicate that the antiapoptotic effect of N. gonorrhoeae in human endocervical epithelial cells results from live infection via expression of host antiapoptotic proteins. Securing an intracellular niche through the inhibition of apoptosis may be an important mechanism utilized by N. gonorrhoeae for microbial survival and immune evasion in cervical epithelial cells. |
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Authors:
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S A Follows; J Murlidharan; P Massari; L M Wetzler; C A Genco |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2009-06-22 |
Journal Detail:
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Title: Infection and immunity Volume: 77 ISSN: 1098-5522 ISO Abbreviation: Infect. Immun. Publication Date: 2009 Sep |
Date Detail:
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Created Date: 2009-08-19 Completed Date: 2009-09-03 Revised Date: 2012-06-27 |
Medline Journal Info:
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Nlm Unique ID: 0246127 Medline TA: Infect Immun Country: United States |
Other Details:
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Languages: eng Pagination: 3602-10 Citation Subset: IM |
Affiliation:
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Department of Microbiology, Section of Molecular Medicine, Boston University School of Medicine, Boston, Massachusetts 02118, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Apoptosis*
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drug effects CASP8 and FADD-Like Apoptosis Regulating Protein / genetics Caspase 3 / physiology Cells, Cultured Cervix Uteri / microbiology*, pathology Female Gonorrhea / immunology Humans Inhibitor of Apoptosis Proteins / genetics, physiology* NF-kappa B / physiology Neisseria gonorrhoeae / pathogenicity* Porins / physiology Receptor-Interacting Protein Serine-Threonine Kinase 2 / genetics Staurosporine / pharmacology |
| Grant Support | |
ID/Acronym/Agency:
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AI048611/AI/NIAID NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/BIRC3 protein, human; 0/CASP8 and FADD-Like Apoptosis Regulating Protein; 0/CFLAR protein, human; 0/Inhibitor of Apoptosis Proteins; 0/NF-kappa B; 0/Porins; 0/porin protein, Neisseria; 62996-74-1/Staurosporine; EC 2.7.11.1/RIPK2 protein, human; EC 2.7.11.1/Receptor-Interacting Protein Serine-Threonine Kinase 2; EC 3.4.22.-/Caspase 3 |
| Comments/Corrections | |
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