ATP Induces IL-1 β Secretion in Neisseria gonorrhoeae-Infected Human Macrophages by a Mechanism Not Related to the NLRP3/ASC/Caspase-1 Axis

Killen Garci�, Gisselle Escobar, Pablo Mendoza, Caroll Beltran, Claudio Perez, Sergio Arancibia, Rolando Vernal, Paula I. Rodas, Claudio Acun�-Castillo, Alejandro Escobar

Resultado de la investigación: Contribución a una revistaArtículo

1 Cita (Scopus)

Resumen

Neisseria gonorrhoeae (Ngo) has developed multiple immune evasion mechanisms involving the innate and adaptive immune responses. Recent findings have reported that Ngo reduces the IL-1β secretion of infected human monocyte-derived macrophages (MDM). Here, we investigate the role of adenosine triphosphate (ATP) in production and release of IL-1β in Ngo-infected MDM. We found that the exposure of Ngo-infected MDM to ATP increases IL-1β levels about ten times compared with unexposed Ngo-infected MDM (P<0.01). However, we did not observe any changes in inflammasome transcriptional activation of speck-like protein containing a caspase recruitment domain (CARD) (ASC, P>0.05) and caspase-1 (CASP1, P>0.05). In addition, ATP was not able to modify caspase-1 activity in Ngo-infected MDM but was able to increase pyroptosis (P>0.01). Notably ATP treatment defined an increase of positive staining for IL-1β with a distinctive intracellular pattern of distribution. Collectively, these data demonstrate that ATP induces IL-1β secretion by a mechanism not related to the NLRP3/ASC/caspase-1 axis and likely is acting at the level of vesicle trafficking or pore formation.

Idioma originalInglés
Número de artículo1258504
PublicaciónMediators of Inflammation
Volumen2016
DOI
EstadoPublicada - 1 ene 2016

Áreas temáticas de ASJC Scopus

  • Inmunología
  • Biología celular

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  • Citar esto

    Garci�, K., Escobar, G., Mendoza, P., Beltran, C., Perez, C., Arancibia, S., Vernal, R., Rodas, P. I., Acun�-Castillo, C., & Escobar, A. (2016). ATP Induces IL-1 β Secretion in Neisseria gonorrhoeae-Infected Human Macrophages by a Mechanism Not Related to the NLRP3/ASC/Caspase-1 Axis. Mediators of Inflammation, 2016, [1258504]. https://doi.org/10.1155/2016/1258504