ArticleScientific reports2016
Reassessing the role of the NLRP3 inflammasome during pathogenic influenza A virus infection via temporal inhibition.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers.
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Who cites it
132 citing papers in PubMed, 219 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
- Gasdermin E is dispensable for H1N1 influenza virus pathogenesis in mice.Microbiology spectrum · 2026Article
- Dissecting Cell Death Pathways in Influenza A Virus Infection: Comparative Insights from Human Models.Viruses · 2026Review
- Antiviral Inflammasomes and How to Find Them.Viruses · 2026Review
- Porcine Epidemic Diarrhea-Virus-Induced Cell Death: Mechanistic Insights and Therapeutic Strategies.Veterinary sciences · 2025Review
- Ninjurin-1 mediates cell lysis and detrimental inflammation of PANoptosis during influenza A virus infection.Signal transduction and targeted therapy · 2025Article
- Pyroptosis in Respiratory Virus Infections: A Narrative Review of Mechanisms, Pathophysiology, and Potential Therapeutic Interventions.Microorganisms · 2025Review
- Gasdermin E deficiency limits inflammation and lung damage during influenza virus infection.Cell death & disease · 2025Article
- TLR7 deficiency enhances inflammation in the URT but reduces LRT immunity following influenza A infection.Scientific reports · 2025Article
- 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
- Review
- Purinergic signaling in the battlefield of viral infections.Purinergic signalling · 2025Review
- The role of cell death pathways in respiratory viral infection and vaccination: two sides of the same coin.Frontiers in immunology · 2025Review
- Cell death in acute lung injury: caspase-regulated apoptosis, pyroptosis, necroptosis, and PANoptosis.Frontiers in pharmacology · 2025Review
- TLR7 Promotes Acute Inflammatory-Driven Lung Dysfunction in Influenza-Infected Mice but Prevents Late Airway Hyperresponsiveness.International journal of molecular sciences · 2024Article
- Influenza, SARS-CoV-2, and Their Impact on Chronic Lung Diseases and Fibrosis: Exploring Therapeutic Options.The American journal of pathology · 2024Review
- Review
- Characterization of a small molecule inhibitor of the NLRP3 inflammasome and its potential use for acute lung injury.Bioorganic chemistry · 2024Article
- Harnessing Endogenous Peptide Compounds as Potential Therapeutics for Severe Influenza.The Journal of infectious diseases · 2024Article
72 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The inflammasome NLRP3 is activated by pathogen associated molecular patterns (PAMPs) during infection, including RNA and proteins from influenza A virus (IAV). However, chronic activation by danger associated molecular patterns (DAMPs) can be deleterious to the host. We show that blocking NLRP3 activation can be either protective or detrimental at different stages of lethal influenza A virus (IAV). Administration of the specific NLRP3 inhibitor MCC950 to mice from one day following IAV challenge resulted in hypersusceptibility to lethality. In contrast, delaying treatment with MCC950 until the height of disease (a more likely clinical scenario) significantly protected mice from severe and highly virulent IAV-induced disease. These findings identify for the first time that NLRP3 plays a detrimental role later in infection, contributing to IAV pathogenesis through increased cytokine production and lung cellular infiltrates. These studies also provide the first evidence identifying NLRP3 inhibition as a novel therapeutic target to reduce IAV disease severity.
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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.