ArticleScientific reports2022
Early IFN-β administration protects cigarette smoke exposed mice against lethal influenza virus infection without increasing lung inflammation.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Article
- Impaired early type I interferon responses to influenza virus infection in aged mice are associated with subsequent increased pulmonary inflammation.GeroScience · 2026Article
- Interferon-β treatment reverses the detrimental effect of B-cell depletion therapy on respiratory virus infection.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- CYP1B1 knockout enhanced IFN-γ production is required but not sufficient for protection of cigarette smoke-exposed mice against lethal influenza virus infection.Frontiers in immunology · 2025Article
- Influenza virus infection exacerbates gene expression related to neurocognitive dysfunction in brains of old mice.Immunity & ageing : I & A · 2024Article
- Lung microvascular occlusion by platelet-rich neutrophil-platelet aggregates promotes cigarette smoke-induced severe flu.JCI insight · 2024Article
- Acute cigarette smoke exposure leads to higher viral infection in human bronchial epithelial cultures by altering interferon, glycolysis and GDF15-related pathways.Respiratory research · 2023Article
- RIG-I agonist SLR10 promotes macrophage M1 polarization during influenza virus infection.Frontiers in immunology · 2023Article
- In Vivo and In Vitro Studies of Cigarette Smoke Effects on Innate Responses to Influenza Virus: A Matter of Models?Viruses · 2022Review
- Severity of neonatal influenza infection is driven by type I interferon and oxidative stress.Mucosal immunology · 2022Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
During influenza A virus (IAV) infection, it is unclear whether type I interferons (IFNs) have defensive antiviral effects or contribute to immunopathology in smokers. We treated nonsmoking (NS) and cigarette smoke (CS)-exposed mice intranasally with early (prophylactic) or late (therapeutic) IFN-β. We compared the mortality and innate immune responses of the treated mice following challenge with IAV. In NS mice, both early and late IFN-β administration decreased the survival rate in mice infected with IAV, with late IFN-β administration having the greatest effect on survival. In contrast, in CS-exposed mice, early IFN-β administration significantly increased survival during IAV infection while late IFN-β administration did not alter mortality. With regards to inflammation, in NS mice, IFN-β administration, especially late administration, significantly increased IAV-induced inflammation and lung injury. Early IFN-β administration to CS-exposed mice did not increase IAV-induced inflammation and lung injury as occurred in NS mice. Our results demonstrate, although IFN-β administration worsens the susceptibility of NS mice to influenza infection with increased immunopathology, early IFN-β administration to CS-exposed mice, which have suppression of the intrinsic IFN response, improved outcomes during influenza infection.
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