ArticleFrontiers in immunology2017
Inhibition of the NOD-Like Receptor Protein 3 Inflammasome Is Protective in Juvenile Influenza A Virus Infection.
Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 83 citations in OpenAlex.
- Inflammasomes in respiratory diseases: from disease pathogenesis to drug development and use of multi-omics.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Ninjurin-1 mediates cell lysis and detrimental inflammation of PANoptosis during influenza A virus infection.Signal transduction and targeted therapy · 2025Article
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- Deep insight into cytokine storm: from pathogenesis to treatment.Signal transduction and targeted therapy · 2025Review
- Jinxin oral liquid reduced lung inflammation in influenza A virus infected mice through inhibiting NOD-like receptor protein 3 pathway.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- NLRP3 regulates epithelial barrier integrity and protects from airway hyperresponsiveness in experimental allergic asthma.Frontiers in immunology · 2025Article
- Analysis of GSDMD-N abnormality promoting neutrophil NETs mediated RA disease through NLRP3-dependent pathway.Frontiers in immunology · 2025Article
- NLRP3 Inflammasomes: Dual Function in Infectious Diseases.Journal of immunology (Baltimore, Md. : 1950) · 2024Review
- A pivotal role for the IL-1β and the inflammasome in preterm labor.Scientific reports · 2024Article
- Article
- Phillyrin ameliorates influenza a virus-induced pulmonary inflammation by antagonizing CXCR2 and inhibiting NLRP3 inflammasome activation.Virology journal · 2023Article
- Interaction among inflammasome, PANoptosise, and innate immune cells in infection of influenza virus: Updated review.Immunity, inflammation and disease · 2023Review
- Pharmacological Inhibition of the NLRP3 Inflammasome: Structure, Molecular Activation, and Inhibitor-NLRP3 Interaction.Pharmacological reviews · 2023Review
- Article
- Influenza a virus triggers acute exacerbation of chronic obstructive pulmonary disease by increasing proinflammatory cytokines secretion via NLRP3 inflammasome activation.Journal of inflammation (London, England) · 2022Article
- The multifaceted roles of NLRP3-modulating proteins in virus infection.Frontiers in immunology · 2022Review
- The cytokine storms of COVID-19, H1N1 influenza, CRS and MAS compared. Can one sized treatment fit all?Cytokine · 2021Review
- The Mechanism behind Influenza Virus Cytokine Storm.Viruses · 2021Review
- Nrf2 activation putatively mediates clinical benefits of low-dose radiotherapy in COVID-19 pneumonia and acute respiratory distress syndrome (ARDS): Novel mechanistic considerations.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2021Review
- The Role of Innate Immunity in Pulmonary Infections.BioMed research international · 2021Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Influenza A virus (IAV) is a significant cause of life-threatening lower respiratory tract infections in children. Antiviral therapy is the mainstay of treatment, but its effectiveness in this age group has been questioned. In addition, damage inflicted on the lungs by the immune response to the virus may be as important to the development of severe lung injury during IAV infection as the cytotoxic effects of the virus itself. A crucial step in the immune response to IAV is activation of the NOD-like receptor protein 3 (NLRP3) inflammasome and the subsequent secretion of the inflammatory cytokines, interleukin-1β (IL-1β), and interleukin-18 (IL-18). The IAV matrix 2 proton channel (M2) has been shown to be an important activator of the NLRP3 inflammasome during IAV infection. We sought to interrupt this ion channel-mediated activation of the NLRP3 inflammasome through inhibition of NLRP3 or the cytokine downstream from its activation, IL-1β. Using our juvenile mouse model of IAV infection, we show that inhibition of the NLRP3 inflammasome with the small molecule inhibitor, MCC950, beginning 3 days after infection with IAV, improves survival in juvenile mice. Treatment with MCC950 reduces NLRP3 levels in lung homogenates, decreases IL-18 secretion into the alveolar space, and inhibits NLRP3 inflammasome activation in alveolar macrophages. Importantly, inhibition of the NLRP3 inflammasome with MCC950 does not impair viral clearance. In contrast, inhibition of IL-1β signaling with the IL-1 receptor antagonist, anakinra, is insufficient to protect juvenile mice from IAV. Our findings suggest that targeting the NLRP3 inflammasome in juvenile IAV infection may improve disease outcomes in this age group.
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