ArticleJournal of immunology (Baltimore, Md. : 1950)2010
Critical role of IL-1 receptor-associated kinase-M in regulating chemokine-dependent deleterious inflammation in murine influenza pneumonia.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
What it found
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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.
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.
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Who cites it
57 citing papers in PubMed, 100 citations in OpenAlex.
- The IL-33-PIN1-IRAK-M axis is critical for type 2 immunity in IL-33-induced allergic airway inflammation.Nature communications · 2018Trial
- Efficacy and safety of intravenous peramivir for treatment of seasonal influenza virus infection.Antimicrobial agents and chemotherapy · 2010Trial
- Identification and Validation of Liver Transplantation-Induced Acute Lung Injury Biomarkers Using a Bioinformatics and Experimental Approach.Annals of transplantation · 2026Article
- Severe Influenza Patients Who Received Ventilator Management During the 2024 to 2025 Major Influenza-Endemic Season in a Tertiary Hospital in Japan.International medical case reports journal · 2025Article
- Modulation of IRAK enzymes as a therapeutic strategy against SARS-CoV-2 induced cytokine storm.Clinical and experimental medicine · 2023Review
- Neutrophils during SARS-CoV-2 infection: Friend or foe?Immunological reviews · 2023Review
- The immune response to COVID-19: Does sex matter?Immunology · 2022Review
- The Immunobiology of Nipah Virus.Microorganisms · 2022Review
- Identification of Nifurtimox and Chrysin as Anti-Influenza Virus Agents by Clinical Transcriptome Signature Reversion.International journal of molecular sciences · 2022Article
- Trends in the management of infectious disease under SARS-CoV-2 era: From pathophysiological comparison of COVID-19 and influenza.World journal of virology · 2021Review
- IRAK-M knockout promotes allergic airway inflammation, but not airway hyperresponsiveness, in house dust mite-induced experimental asthma model.Journal of thoracic disease · 2021Article
- An Assessment on Impact of COVID-19 Infection in a Gender Specific Manner.Stem cell reviews and reports · 2021Review
- The Modulatory Activity of Tryptophan Displaying Nanodevices on Macrophage Activation for Preventing Acute Lung Injury.Frontiers in immunology · 2021Article
- RGS10 Reduces Lethal Influenza Infection and Associated Lung Inflammation in Mice.Frontiers in immunology · 2021Article
- NMP4 regulates the innate immune response to influenza A virus infection.Mucosal immunology · 2021Article
- Progesterone Receptor Signaling Selectively Modulates Cytokine-Induced Global Gene Expression in Human Cervical Stromal Cells.Frontiers in genetics · 2020Article
- Excessive neutrophil levels in the lung underlie the age-associated increase in influenza mortality.Mucosal immunology · 2019Article
- Influenza Virus Infections and Cellular Kinases.Viruses · 2019Review
- Cancer; an induced disease of twentieth century! Induction of tolerance, increased entropy and 'Dark Energy': loss of biorhythms (Anabolism v. Catabolism).Clinical and translational medicine · 2018Article
- Stimulation of alpha2-adrenergic receptors impairs influenza virus infection.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Influenza virus is a common cause of respiratory infection and morbidity, which is often due to deleterious host immune responses directed against the pathogen. We investigated the role of IL-1 receptor-associated kinase-M (IRAK-M), an inhibitor of MyD88-dependent TLR signaling, in modulating the innate inflammatory response during influenza pneumonia using a murine model. The intranasal administration of influenza resulted in the upregulation of IRAK-M mRNA and protein levels in the lungs within 2 d after infectious challenge. Pulmonary influenza infection in mice deficient in IRAK-M (IRAK-M(-/-)) resulted in substantially increased mortality compared with similarly treated wild-type animals. Increased mortality in IRAK-M(-/-) mice was associated with enhanced early influx of neutrophils, high permeability edema, apoptosis of lung epithelial cells, markedly increased expression of inflammatory cytokines/chemokines, and release of neutrophil-derived enzymes, including myeloperoxidase and neutrophil elastase. Early viral clearance was not different in mutant mice, whereas viral titers in lungs and blood were significantly higher in IRAK-M(-/-) mice compared with wild-type animals. Increased lethality observed in IRAK-M(-/-) mice after influenza challenge was abrogated by Ab-mediated blockade of CXCR2. Collectively, our findings indicate that IRAK-M is critical to preventing deleterious neutrophil-dependent lung injury during influenza infection of the respiratory tract.
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What OpenQuestion holds
Registered trials
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.