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Follows SA et al. - Results indicate that the anti-apoptotic effect of N. gonorrhoeae in human endocervical epithelial cells results from live infection via expression of host anti-apoptotic 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.

Exclusive Author Commentary
C. A. Genco, 07/09/09

It has long been known that significant subsets of women with ?gonococcal infection are asymptomatic, producing a reservoir of organisms to allow ongoing progression of this disease. ?The reason for this lack of inflammation inducing signs and symptoms ?of infection has been unclear. It was debated whether the lack of ?inflammation was due to an active inhibition of certain innate and ?acquired immune responses. We explored one potential reason for this ?lack of a response by determining whether in cervical cells this organism can actively ?inhibit apoptosis, a known signal that can initiate a cascade of ?events leading to cell activation, inflammatory mediator production ?and cell recruitment. We ?found that live gonococci could protect cervical cell lines from ?apoptosis and that this was due to a direct stimulation of the cells, ?induction of NF-kB nuclear translocation and up regulation of antiapoptotic genes including bfl1, cIAP-2 and c-FLIP. This may be one ?mechanism by which this organism inhibits apoptosis and masks its presence in the cervical and vaginal mucosa where these cells reside.

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