ArticleImmunology and cell biology2021
Interleukin-1β exacerbates disease and is a potential therapeutic target to reduce pulmonary inflammation during severe influenza A virus infection.
Article in Immunology and cell biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 48 citations in OpenAlex.
- Pseudorabies virus infection induces IRF1-dependent PANoptosis to provoke the excessive release of HMGB1 and IL-1β.Communications biology · 2026Article
- Time-Resolved Transcriptomic Profiling of Chandipura Virus Infection Reveals Dynamic Host Responses and Host-Directed Therapeutic Targets.International journal of molecular sciences · 2026Article
- Therapeutic Efficacy of the Supersulfide Donor NAC-S2 in Influenza Virus Pneumonia via Suppression of Excessive Inflammatory Responses.Microbiology and immunology · 2026Article
- Dissecting Cell Death Pathways in Influenza A Virus Infection: Comparative Insights from Human Models.Viruses · 2026Review
- Family-wise resistance to infectious salmon anemia suggests that early systemic recognition protects against disease but not viral transcription.Frontiers in immunology · 2026Article
- Hyperinflammation and immunomodulation in influenza, SARS-CoV-2 and syncytial respiratory virus infection in adults: from innate immune responses and biomarkers to clinical and therapeutic implications.Frontiers in microbiology · 2026Review
- Bridging pDCs and cDCs: The Identity of Transitional Dendritic Cells.Immunological reviews · 2025Review
- Ninjurin-1 mediates cell lysis and detrimental inflammation of PANoptosis during influenza A virus infection.Signal transduction and targeted therapy · 2025Article
- IL-1β drives SARS-CoV-2-induced disease independently of the inflammasome and pyroptosis signalling.Cell death and differentiation · 2025Article
- Gasdermin E deficiency limits inflammation and lung damage during influenza virus infection.Cell death & disease · 2025Article
- Deep insight into cytokine storm: from pathogenesis to treatment.Signal transduction and targeted therapy · 2025Review
- NLRP3 deficiency abrogates silica-induced neutrophil infiltration, pulmonary damage and fibrosis.Respiratory research · 2025Article
- Article
- The Role of Inflammation in the Pathogenesis of Viral Respiratory Infections.Microorganisms · 2024Review
- The dichotomic role of cytokines in aging.Biogerontology · 2024Review
- Review
- Harnessing Endogenous Peptide Compounds as Potential Therapeutics for Severe Influenza.The Journal of infectious diseases · 2024Article
- NLRP3 Inflammasomes: Dual Function in Infectious Diseases.Journal of immunology (Baltimore, Md. : 1950) · 2024Review
- Recombinant Hemagglutinin Protein from H9N2 Avian Influenza Virus Exerts Good Immune Effects in Mice.Microorganisms · 2024Article
- Melatonin improves influenza virus infection-induced acute exacerbation of COPD by suppressing macrophage M1 polarization and apoptosis.Respiratory research · 2024Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperinflammatory responses including the production of NLRP3-dependent interleukin (IL)-1β is a characteristic feature of severe and fatal influenza A virus (IAV) infections. The NLRP3 inflammasome has been shown to play a temporal role during severe IAV immune responses, with early protective and later detrimental responses. However, the specific contribution of IL-1β in modulating IAV disease in vivo is currently not well defined. Here, we identified that activation of NLRP3-dependent IL-1β responses occurs rapidly following HKx31 H3N2 infection, prior to the onset of severe IAV disease. Mature IL-1β was detectable in vivo in both hemopoietic and nonhemopoietic cells. Significantly, therapeutic inhibition of IL-1β in the airways with intranasal anti-IL-1β antibody treatment from day 3 postinfection, corresponding to the onset of clinical signs of disease, significantly prolonged survival and reduced inflammation in the airways. Importantly, early targeting of IL-1β from day 1 postinfection also improved survival. Together, these studies specifically define a role for IL-1β in contributing to the development of hyperinflammation and disease and indicate that targeting IL-1β is a potential therapeutic strategy for severe IAV infections.
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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.