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

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Miniatura
Fecha
2016
Profesor/a Guía
Facultad/escuela
Idioma
en
Título de la revista
ISSN de la revista
Título del volumen
Editor
HINDAWI PUBLISHING
Nombre de Curso
Licencia CC
Licencia CC
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-1 beta secretion of infected human monocyte-derived macrophages (MDM). Here, we investigate the role of adenosine triphosphate (ATP) in production and release of IL-1 beta in Ngo-infected MDM. We found that the exposure of Ngo-infected MDM to ATP increases IL-1 beta 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-1 beta with a distinctive intracellular pattern of distribution. Collectively, these data demonstrate that ATP induces IL-1 beta 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.
Notas
Indexación: Web of Science y Scopus
Palabras clave
KAPPA-B ACTIVATION, PORPHYROMONAS-GINGIVALIS, NLRP3 INFLAMMASOME, INTRACELLULAR BACTERIA, EXTRACELLULAR ATP, EPITHELIAL-CELLS, HUMAN PHAGOCYTES, P2X(7) RECEPTOR, DEATH, EXPRESSION
Citación
Mediators of Inflammation, vol. 2016, Article ID 1258504
DOI
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