ArticleRespiratory research2020
Host DNA released by NETosis in neutrophils exposed to seasonal H1N1 and highly pathogenic H5N1 influenza viruses.
Article in Respiratory research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 25 citations in OpenAlex.
- Heterogeneous viral-host response at single-cell resolution and viral adaptive mutational atlas in birds and mammals upon H5 influenza virus infection.National science review · 2026Article
- Cell death crosstalk in NET-Driven inflammation: mechanisms, disease contexts, and therapeutic perspectives.Biomarker research · 2026Review
- Metatranscriptomics uncovers host immune and microbiome signatures specific to and shared between human metapneumovirus and respiratory syncytial virus infections in children.Virologica Sinica · 2026Article
- Review
- Neutrophil Dynamics in Viral Infections: Drivers of Inflammation and Targets for Pro-Resolving Therapies.Journal of innate immunity · 2026Review
- Hippo pathway and NLRP3-driven NETosis in macrophages: Mechanisms of viral pneumoniaaggravation.Cell death discovery · 2025Article
- Deep insight into cytokine storm: from pathogenesis to treatment.Signal transduction and targeted therapy · 2025Review
- Treatment with lipoxin AInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Article
- Treatment with lipoxin A 4 improves influenza A infection outcome through macrophage reprogramming, anti-inflammatory and pro-resolutive responses.Research square · 2024Article
- Gasdermin D promotes influenza virus-induced mortality through neutrophil amplification of inflammation.Nature communications · 2024Article
- Detection of Granzyme B-associated Binding Targets in Peripheral Blood Samples of Hosts in Sickness and in Health Using a Granzyme B-like Peptide Fluorescent Conjugate (GP1R).Journal of fluorescence · 2024Article
- Interaction among inflammasome, PANoptosise, and innate immune cells in infection of influenza virus: Updated review.Immunity, inflammation and disease · 2023Review
- NETosis and SARS-COV-2 infection related thrombosis: a narrative review.Thrombosis journal · 2022Article
- Role of Extracellular Trap Release During Bacterial and Viral Infection.Frontiers in microbiology · 2022Review
- Mechanistic Understanding of Lung Inflammation: Recent Advances and Emerging Techniques.Journal of inflammation research · 2022Review
- The Roles of Neutrophils in Cytokine Storms.Viruses · 2021Review
- Neutrophils at the crossroads of acute viral infections and severity.Molecular aspects of medicine · 2021Review
- Increased levels of NETosis in myeloproliferative neoplasms are not linked to thrombotic events.Blood advances · 2021Article
- A Fragile Balance: Does Neutrophil Extracellular Trap Formation Drive Pulmonary Disease Progression?Cells · 2021Review
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 3 countries.
Funding
Abstract
backgroundNeutrophil is of the most abundant number in human immune system. During acute influenza virus infection, neutrophils are already active in the early phase of inflammation - a time in which clinical biopsy or autopsy material is not readily available. However, the role of neutrophil in virus infection is not well understood. Here, we studied the role of neutrophil in host defense during influenza A virus infection, specifically assessing if it contributes to the differential pathogenesis in H5N1 disease.
methodsNeutrophils were freshly isolated from healthy volunteers and subjected to direct influenza H1N1 and H5N1 virus infection in vitro. The ability of the naïve neutrophils to infiltrate from the basolateral to the apical phase of the influenza virus infected alveolar epithelium was assessed. The viral replication, innate immune responses and Neutrophil extracellular trap (NET) formation of neutrophils upon influenza virus infection were evaluated.
resultsOur results demonstrated that influenza virus infected alveolar epithelium allowed neutrophil transmigration. Significantly more neutrophils migrated across the H5N1 influenza virus infected the epithelium than the counterpart infected by the seasonal influenza H1N1 virus infected. Neutrophils were equally susceptible to H5N1 and H1N1 virus infection with similar viral gene transcription. Productive replication was observed in H5N1 infected neutrophils. H5N1 induced higher cytokine and chemokine gene transcription than H1N1 infected neutrophils, including TNF-α, IFN-β, CXCL10, MIP-1α and IL-8. This inferred a more intense inflammatory response posed by H5N1 than H1N1 virus. Strikingly, NADPH oxidase-independent NET formation was only observed in H1N1 infected neutrophils at 6 hpi while no NET formation was observed upon H5N1 infection.
conclusionOur data is the first to demonstrate that NET formation is abrogated in H5N1 influenza virus infection and might contribute to the severity of H5N1 disease.
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