Influenza A Virus NS1 Protein Inhibits the NLRP3 Inflammasome
- Authors
- Cheong, Woo-Chang; Kang, Hye-Ri; Yoon, Hyunyee; Kang, Suk-Jo; Ting, Jenny P. -Y.; Song, Moon Jung
- Issue Date
- 15-5월-2015
- Publisher
- PUBLIC LIBRARY SCIENCE
- Citation
- PLOS ONE, v.10, no.5
- Indexed
- SCIE
SCOPUS
- Journal Title
- PLOS ONE
- Volume
- 10
- Number
- 5
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/93548
- DOI
- 10.1371/journal.pone.0126456
- ISSN
- 1932-6203
- Abstract
- The inflammasome is a molecular platform that stimulates the activation of caspase-1 and the processing of pro-interleukin (IL)-1 beta 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-1 alpha 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-kappa B (NF-kappa B), 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-kappa B, leading to a reduction in the levels of inflammatory cytokines as a viral immune evasion strategy.
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