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Differential Response of Primary and Immortalized CD4(+) T Cells to Neisseria gonorrhoeae-Induced Cytokines Determines the Effect on HIV-1 Replication

To compare the effect of gonococcal co-infection on immortalized versus primary CD4(+) T cells the Jurkat cell line or freshly isolated human CD4(+) T cells were infected with the HIV-1 X4 strain NL4-3. These cells were exposed to whole gonococci, supernatants from gonococcal-infected PBMCs, or N. g...

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Detalles Bibliográficos
Autores principales: Dobson-Belaire, Wendy N., Cochrane, Alan, Ostrowski, Mario A., Gray-Owen, Scott D.
Formato: Texto
Lenguaje:English
Publicado: Public Library of Science 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3081295/
https://www.ncbi.nlm.nih.gov/pubmed/21526113
http://dx.doi.org/10.1371/journal.pone.0018133
Descripción
Sumario:To compare the effect of gonococcal co-infection on immortalized versus primary CD4(+) T cells the Jurkat cell line or freshly isolated human CD4(+) T cells were infected with the HIV-1 X4 strain NL4-3. These cells were exposed to whole gonococci, supernatants from gonococcal-infected PBMCs, or N. gonorrhoeae-induced cytokines at varying levels. Supernatants from gonococcal-infected PBMCs stimulated HIV-1 replication in Jurkat cells while effectively inhibiting HIV-1 replication in primary CD4(+) T cells. ELISA-based analyses revealed that the gonococcal-induced supernatants contained high levels of proinflammatory cytokines that promote HIV-1 replication, as well as the HIV-inhibitory IFNα. While all the T cells responded to the HIV-stimulatory cytokines, albeit to differing degrees, the Jurkat cells were refractory to IFNα. Combined, these results indicate that N. gonorrhoeae elicits immune-modulating cytokines that both activate and inhibit HIV-production; the outcome of co-infection depending upon the balance between these opposing signals.