Extracellular nucleoprotein exacerbates influenza virus pathogenesis by activating Toll-like receptor 4 and the NLRP3 inflammasome

Cited 9 time in scopus
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Title
Extracellular nucleoprotein exacerbates influenza virus pathogenesis by activating Toll-like receptor 4 and the NLRP3 inflammasome
Author(s)
Chang Ung Kim; Yu-Jin Jeong; Pureum Lee; Moo-Seung Lee; J H Park; Y S Kim; Doo-Jin Kim
Bibliographic Citation
Cellular & Molecular Immunology, vol. 19, no. 6, pp. 715-725
Publication Year
2022
Abstract
Host immune responses, such as those initiated by pattern recognition receptor (PRR) activation, are important for viral clearance and pathogenesis. However, little is known about the interactions of viral proteins with surface PRRs or, more importantly, the association of innate immune activation with viral pathogenesis. In this study, we showed that internal influenza virus proteins were released from infected cells. Among these proteins, nucleoprotein (NP) played a critical role in viral pathogenesis by stimulating neighboring cells through toll-like receptor (TLR)2, TLR4, and the NLR family pyrin domain containing 3 (NLRP3) inflammasome. Through the activation of these PRRs, NP induced the production of interleukin (IL)-1β and IL-6, which subsequently led to the induction of trypsin. Trypsin induced by NP increased the infectivity of influenza virus, leading to increases in viral replication and pathology upon subsequent viral infection. These results reveal the role of released NP in influenza pathogenesis and highlight the importance of the interactions of internal viral proteins with PRRs in the extracellular compartment during viral pathogenesis.
Keyword
Influenza virusViral protein releaseNucleoproteinToll-like receptorCyotkine-trypsin cycle
ISSN
1672-7681
Publisher
Chin Society Immunology
DOI
http://dx.doi.org/10.1038/s41423-022-00862-5
Type
Article
Appears in Collections:
Division of Research on National Challenges > Environmental diseases research center > 1. Journal Articles
Division of Research on National Challenges > Infectious Disease Research Center > 1. Journal Articles
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