ArticleVirulence2022
H1N1 influenza virus dose dependent induction of dysregulated innate immune responses and STAT1/3 activation are associated with pulmonary immunopathological damage.
Article in Virulence, 2022. 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, 24 citations in OpenAlex.
- GPR84 aggravates lung inflammation through activating ZBP1-PANoptosome mediated PANoptosis following IAV infection.Cell death discovery · 2026Article
- Immune cell disorder in viral pneumonia.Journal of translational medicine · 2026Review
- LUCAT1 drives arecoline-induced head and neck cancer progression via STAT1-mediated transcriptional regulation.Cellular & molecular biology letters · 2026Article
- The "cytokine storm" in infection and sepsis: win the battle but lose the war.Military Medical Research · 2026Review
- Neutrophil Dynamics in Viral Infections: Drivers of Inflammation and Targets for Pro-Resolving Therapies.Journal of innate immunity · 2026Review
- Post-translational modification networks as master regulators of influenza virus replication, host adaptation, and immune evasion.Frontiers in immunology · 2026Review
- Article
- Deciphering the antiviral mechanisms of Fangqin Qinggan decoction against influenza A virus: a multi-omics and machine learning approach.Chinese medicine · 2025Article
- Multiomics analysis unveils key biomarkers during dynamic progress of IAV infection in mice.Frontiers in immunology · 2025Article
- Investigation of the effect and mechanisms of moxa smoke in the treatment of Influenza A Virus (IAV) infection.PloS one · 2025Article
- The regulatory roles of STAT3 protein in the pathogenesis of viral infections.Frontiers in cellular and infection microbiology · 2025Review
- Viral-associated septic shock in pediatric pneumonia: a retrospective analysis of pathogen-specific risks and comparative clinical features with bacterial sepsis.Frontiers in pediatrics · 2025Article
- Functional Involvement of Signal Transducers and Activators of Transcription in the Pathogenesis of Influenza A Virus.International journal of molecular sciences · 2024Review
- Novel Core Gene Signature Associated with Inflammation-to-Metaplasia Transition in Influenza A Virus-Infected Lungs.International journal of molecular sciences · 2024Article
- Influenza A virus infection activates STAT3 to enhance SREBP2 expression, cholesterol biosynthesis, and virus replication.iScience · 2024Article
- Defining Parameters That Modulate Susceptibility and Protection to Respiratory Murine Coronavirus MHV1 Infection.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Protective effect of Haoqin Qingdan decoction on pulmonary and intestinal injury in mice with influenza viral pneumonia.Frontiers in pharmacology · 2024Article
- Pathogenicity and virulence of influenza.Virulence · 2023Review
- Advances in immune response to pulmonary infection: Nonspecificity, specificity and memory.Chronic diseases and translational medicine · 2023Review
- Inhibition of H1N1 byFood science & nutrition · 2023Article
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Influenza A virus (IAV) infection poses a substantial challenge and causes high morbidity and mortality. Exacerbated pulmonary inflammatory responses are the major causes of extensive diffuse alveolar immunopathological damage. However, the relationship between the extent of cytokine storm, neutrophils/macrophages infiltration, and different IAV infection dose and time still needs to be further elucidated, and it is still unclear whether the signal transduction and transcriptional activator 1/3 (STAT1/3) signalling pathway plays a beneficial or detrimental role. Here, we established a mouse model of high- and low-dose pH1N1 infection. We found that pH1N1 infection induced robust and early pathological damage and cytokine storm in an infection dose- and time-dependent manner. High-dose pH1N1 infection induced massive and sustained recruitment of neutrophils as well as a higher ratio of M1:M2, which may contribute to severe lung immunopathological damage. pH1N1 infection activated dose- and time-dependent STAT1 and STAT3. Inhibition of STAT1 and/or STAT3 aggravated low-dose pH1N1 infection, induced lung damage, and decreased survival rate. Appropriate activation of STAT1/3 provided survival benefits and pathological improvement during low-dose pH1N1 infection. These results demonstrate that high-dose pH1N1 infection induces robust and sustained neutrophil infiltration, imbalanced macrophage polarization, excessive and earlier cytokine storm, and STAT1/3 activation, which are associated with pulmonary dysregulated proinflammatory responses and progress of acute lung injury. The severe innate immune responses may be the threshold at which protective functions give way to immunopathology, and assessing the magnitude of host innate immune responses is necessary in adjunctive immunomodulatory therapy for alleviating influenza-induced pneumonia.
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