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dc.contributor.authorGarciá K.
dc.contributor.authorEscobar G.
dc.contributor.authorMendoza P.
dc.contributor.authorBeltran C.
dc.contributor.authorPerez C.
dc.contributor.authorArancibia S.
dc.contributor.authorVernal R.
dc.contributor.authorRodas P.I.
dc.contributor.authorAcunã-Castillo C.
dc.contributor.authorEscobar A.
dc.date.accessioned2020-09-02T22:18:44Z
dc.date.available2020-09-02T22:18:44Z
dc.date.issued2016
dc.identifier10.1155/2016/1258504
dc.identifier.citation2016, , -
dc.identifier.issn09629351
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4601
dc.descriptionNeisseria 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. © 2016 Killen Garciá et al.
dc.language.isoen
dc.publisherHindawi Limited
dc.titleATP Induces IL-1 β Secretion in Neisseria gonorrhoeae-Infected Human Macrophages by a Mechanism Not Related to the NLRP3/ASC/Caspase-1 Axis
dc.typeArticle


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