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Volumn 54, Issue , 2018, Pages 80-85

An update on the NLRP3 inflammasome and influenza: the road to redemption or perdition?

Author keywords

[No Author keywords available]

Indexed keywords

CRYOPYRIN; INFLAMMASOME; INTERLEUKIN 18; INTERLEUKIN 1BETA; RNA;

EID: 85049318091     PISSN: 09527915     EISSN: 18790372     Source Type: Journal    
DOI: 10.1016/j.coi.2018.06.005     Document Type: Review
Times cited : (45)

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    • This study identifies IRF1 as a key upstream regulator of inflammasome and cell death during IAV infection, with IRF-deficient cells demonstrating reduced inflammation and cell death.
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    • This study defines the metabolic response in IAV-infected humans and primary respiratory cells, identifying a potential protective therapy by targeting metabolic mitochondrial reprogramming. The implications of this study may be that reducing metabolic function reduces priming (i.e. signal 1) of inflammasome function.
    • Smallwood, H.S., Duan, S., Morfouace, M., Rezinciuc, S., Shulkin, B.L., Shelat, A., Zink, E.E., Milasta, S., Bajracharya, R., Oluwaseum, A.J., et al. Targeting metabolic reprogramming by influenza infection for therapeutic intervention. Cell Rep 19 (2017), 1640–1653 This study defines the metabolic response in IAV-infected humans and primary respiratory cells, identifying a potential protective therapy by targeting metabolic mitochondrial reprogramming. The implications of this study may be that reducing metabolic function reduces priming (i.e. signal 1) of inflammasome function.
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    • Reassessing the role of the NLRP3 inflammasome during pathogenic influenza A virus infection via temporal inhibition
    • The first study to identify the therapeutic potential of targeting the NLRP3 inflammasome during severe and lethal IAV infection. It also demonstrated the temporal role of the NLRP3 inflammasome, mediating both protective and detrimental inflammation during the time course of IAV pathogenesis.
    • Tate, M.D., Ong, J.D., Dowling, J.K., McAuley, J.L., Robertson, A.B., Latz, E., Drummond, G.R., Cooper, M.A., Hertzog, P.J., Mansell, A., Reassessing the role of the NLRP3 inflammasome during pathogenic influenza A virus infection via temporal inhibition. Sci Rep, 6, 2016, 27912 The first study to identify the therapeutic potential of targeting the NLRP3 inflammasome during severe and lethal IAV infection. It also demonstrated the temporal role of the NLRP3 inflammasome, mediating both protective and detrimental inflammation during the time course of IAV pathogenesis.
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    • The H7N9 influenza A virus infection results in lethal inflammation in the mammalian host via the NLRP3-caspase-1 inflammasome
    • This study, for the first time, demonstrated thein vivo effect of inflammasome activation in response to pathogenic H7N9 infection and highlights the importance of the NLRP3 inflammasome protecting against a pandemic strain of IAV.
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