{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T21:23:40Z","timestamp":1792185820734,"version":"4.4.0"},"reference-count":69,"publisher":"American Society for Microbiology","issue":"9","license":[{"start":{"date-parts":[[2009,9,1]],"date-time":"2009-09-01T00:00:00Z","timestamp":1251763200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2009,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            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\n            <jats:italic>Neisseria gonorrhoeae<\/jats:italic>\n            can either inhibit or induce apoptosis.\n            <jats:italic>N. gonorrhoeae<\/jats:italic>\n            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            <jats:italic>N. gonorrhoeae<\/jats:italic>\n            infection in human endocervical epithelial cells (End\/E6E7 cells). We first established that\n            <jats:italic>N. gonorrhoeae<\/jats:italic>\n            strain FA1090B failed to induce cell death in End\/E6E7 cells. Subsequently, we demonstrated that stimulation with\n            <jats:italic>N. gonorrhoeae<\/jats:italic>\n            protected these cells from staurosporine (STS)-induced apoptosis. Importantly, only End\/E6E7 cells incubated with live bacteria and in direct association with\n            <jats:italic>N. gonorrhoeae<\/jats:italic>\n            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            <jats:italic>N. gonorrhoeae<\/jats:italic>\n            induced NF-\u03baB activation and resulted in increased gene expression of the NF-\u03baB-regulated antiapoptotic genes\n            <jats:italic>bfl-1<\/jats:italic>\n            ,\n            <jats:italic>cIAP-2<\/jats:italic>\n            , and\n            <jats:italic>c-FLIP<\/jats:italic>\n            . Furthermore, cIAP-2 protein levels also increased in End\/E6E7 cells incubated with gonococci. Collectively, our results indicate that the antiapoptotic effect of\n            <jats:italic>N. gonorrhoeae<\/jats:italic>\n            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            <jats:italic>N. gonorrhoeae<\/jats:italic>\n            for microbial survival and immune evasion in cervical epithelial cells.\n          <\/jats:p>","DOI":"10.1128\/iai.01366-08","type":"journal-article","created":{"date-parts":[[2009,6,23]],"date-time":"2009-06-23T00:59:41Z","timestamp":1245718781000},"page":"3602-3610","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":28,"title":["<i>Neisseria gonorrhoeae<\/i>\n            Infection Protects Human Endocervical Epithelial Cells from Apoptosis via Expression of Host Antiapoptotic Proteins"],"prefix":"10.1128","volume":"77","author":[{"given":"S. A.","family":"Follows","sequence":"first","affiliation":[{"name":"Department of Microbiology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J.","family":"Murlidharan","sequence":"additional","affiliation":[{"name":"Department of Microbiology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P.","family":"Massari","sequence":"additional","affiliation":[{"name":"Department of Medicine, Section of Infectious Diseases"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L. M.","family":"Wetzler","sequence":"additional","affiliation":[{"name":"Department of Microbiology"},{"name":"Department of Medicine, Section of Infectious Diseases"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C. 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