Influenza A virus NS1 protein inhibits the NLRP3 inflammasome

Woo Chang Cheong, Hye Ri Kang, Hyunyee Yoon, Suk Jo Kang, Jenny P.Y. Ting, Moon Jung Song

Research output: Contribution to journalArticlepeer-review

65 Citations (Scopus)


The inflammasome is a molecular platform that stimulates the activation of caspase-1 and the processing of pro-interleukin (IL)-1β and pro-IL-18 for secretion. The NOD-like receptor family, pyrin domain containing 3 (NLRP3) protein is activated by diverse molecules and pathogens, leading to the formation of the NLRP3 inflammasome. Recent studies showed that the NLRP3 inflammasome mediates innate immunity against influenza A virus (IAV) infection. In this study, we investigated the function of the IAV non-structural protein 1 (NS1) in the modulation of NLRP3 inflammasome. We found that NS1 proteins derived from both highly pathogenic and low pathogenic strains efficiently decreased secretion of IL-1β and IL-18 from THP-1 cells treated with LPS and ATP. NS1 overexpression significantly impaired the transcription of proinflammatory cytokines by inhibiting transactivation of the nuclear factor-κB (NF-κB), a major transcription activator. Furthermore, NS1 physically interacted with endogenous NLRP3 and activation of the NLRP3 inflammasome was abrogated in NS1-expressing THP-1 cells. These findings suggest that NS1 downregulates NLRP3 inflammasome activation by targeting NLRP3 as well as NF-κB, leading to a reduction in the levels of inflammatory cytokines as a viral immune evasion strategy.

Original languageEnglish
Article number0126456
JournalPloS one
Issue number5
Publication statusPublished - 2015 May 15

Bibliographical note

Publisher Copyright:
© 2015 Cheong et al.

ASJC Scopus subject areas

  • General


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