Evidence map›Paper›PMID 35459853›Full record

ArticleCellular & molecular immunology2022

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

Chang-Ung Kim, Yu-Jin Jeong, Pureum Lee, Moo-Seung Lee, Jong-Hwan Park, Young-Sang Kim, Doo-Jin Kim

Open access · bronzeAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.7field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 31 citations in OpenAlex.

  1. Myeloid TLR2 signaling amplifies immunopathology in influenza-infected murine neonates.American journal of respiratory cell and molecular biology · 2026
    Article
  2. Article
  3. Article
  4. Review
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  6. Article
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  8. Innate immune role of IL-6 in influenza a virus pathogenesis.Frontiers in cellular and infection microbiology · 2025
    Review
  9. Article
  10. Evasion of the Antiviral Innate Immunity by PRV.International journal of molecular sciences · 2024
    Review
  11. NLRP3 Inflammasomes: Dual Function in Infectious Diseases.Journal of immunology (Baltimore, Md. : 1950) · 2024
    Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Regulation and functions of the NLRP3 inflammasome in RNA virus infection.Frontiers in cellular and infection microbiology · 2023
    Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 1 country.

Chang-Ung KimInfectious Disease Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, South Korea.
Yu-Jin JeongEnvironmental Diseases Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, South Korea.
Pureum LeeEnvironmental Diseases Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, South Korea.
Moo-Seung LeeEnvironmental Diseases Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, South Korea.
Jong-Hwan ParkCollege of Veterinary Medicine, Chonnam National University, Gwangju, South Korea.
Young-Sang KimDepartment of Biochemistry, Chungnam National University, Daejeon, South Korea. young@cnu.ac.kr.
Doo-Jin KimInfectious Disease Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, South Korea. golddj@kribb.re.kr.
Korea Research Institute of Bioscience and Biotechnology · KRKorea University of Science and Technology · KRChonnam National University · KRChungnam National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Influenza, HumanOrthomyxoviridaeToll-Like Receptor 4HumansInflammasomesInterleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinNucleoproteinsTrypsinInflammasomesInterleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanNucleoproteinsTLR4 protein, humanToll-Like Receptor 4TrypsinCyotkine-trypsin cycleInfluenza virusNucleoproteinToll-like receptorViral protein release

Identifiers

PMID35459853
PMCPMC9026019
OpenAlexW4224257306

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.