Abstract:
:The nucleotide-binding domain and leucine-rich-repeat-containing (NLR) family of pattern-recognition molecules mediate host immunity to various pathogenic stimuli. However, in vivo evidence for the involvement of NLR proteins in viral sensing has not been widely investigated and remains controversial. As a test of the physiologic role of the NLR molecule NLRP3 during RNA viral infection, we explored the in vivo role of NLRP3 inflammasome components during influenza virus infection. Mice lacking Nlrp3, Pycard, or caspase-1, but not Nlrc4, exhibited dramatically increased mortality and a reduced immune response after exposure to the influenza virus. Utilizing analogs of dsRNA (poly(I:C)) and ssRNA (ssRNA40), we demonstrated that an NLRP3-mediated response could be activated by RNA species. Mechanistically, NLRP3 inflammasome activation by the influenza virus was dependent on lysosomal maturation and reactive oxygen species (ROS). Inhibition of ROS induction eliminated IL-1beta production in animals during influenza infection. Together, these data place the NLRP3 inflammasome as an essential component in host defense against influenza infection through the sensing of viral RNA.
journal_name
Immunityjournal_title
Immunityauthors
Allen IC,Scull MA,Moore CB,Holl EK,McElvania-TeKippe E,Taxman DJ,Guthrie EH,Pickles RJ,Ting JPdoi
10.1016/j.immuni.2009.02.005subject
Has Abstractpub_date
2009-04-17 00:00:00pages
556-65issue
4eissn
1074-7613issn
1097-4180pii
S1074-7613(09)00139-3journal_volume
30pub_type
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