ArticleRespiratory research2016
Inflammation and emphysema in cigarette smoke-exposed mice when instilled with poly (I:C) or infected with influenza A or respiratory syncytial viruses.
Article in Respiratory research, 2016. 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, 27 citations in OpenAlex.
- Preclinical models of COPD: a state of the art review.The European respiratory journal · 2026Review
- A colon mimetic screening approach reveals Lactobacillus fermentum as a microbiome-based therapy for COPD.NPJ biofilms and microbiomes · 2026Article
- New approaches to uncover COPD pathobiology and develop therapies.JCI insight · 2026Review
- Dynamic changes of immune cells and therapeutic responses in experimental models of COPD.Frontiers in immunology · 2026Review
- circ-0001454 alleviates asthma airway inflammation and remodeling via sponging miR-770-5p and regulating cbl-b.Frontiers in cell and developmental biology · 2025Article
- Molecular Mechanisms of N-Acetylcysteine in RSV Infections and Air Pollution-Induced Alterations: A Scoping Review.International journal of molecular sciences · 2024Article
- Persistence of emphysema following cessation of cigarette smoke exposure requires a susceptibility factor.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- TGF-β1 and TGF-βR1 variants are associated with clinical outcomes in smoking-related head and neck cancer patients treated with chemoradiation through modulating microRNA-mediated regulation.Cancer immunology, immunotherapy : CII · 2024Article
- The Genetics behind Sulfation: Impact on Airway Remodeling.Journal of personalized medicine · 2024Review
- Lung microvascular occlusion by platelet-rich neutrophil-platelet aggregates promotes cigarette smoke-induced severe flu.JCI insight · 2024Article
- Recombinant Human HAPLN1 Mitigates Pulmonary Emphysema by Increasing TGF-β Receptor I and Sirtuins Levels in Human Alveolar Epithelial Cells.Molecules and cells · 2023Article
- RIG-I agonist SLR10 promotes macrophage M1 polarization during influenza virus infection.Frontiers in immunology · 2023Article
- Modeling the effects of cigarette smoke extract on influenza B virus infections in mice.Frontiers in immunology · 2023Article
- Article
- Molecular Mechanisms of RSV and Air Pollution Interaction: A Scoping Review.International journal of molecular sciences · 2022Article
- In Vivo and In Vitro Studies of Cigarette Smoke Effects on Innate Responses to Influenza Virus: A Matter of Models?Viruses · 2022Review
- Effects of Cigarette Smoking on Influenza Virus/Host Interplay.Pathogens (Basel, Switzerland) · 2021Review
- Inflammatory effects of particulate matter air pollution.Environmental science and pollution research international · 2020Review
- Influenza in High-Risk Hosts-Lessons Learned from Animal Models.Cold Spring Harbor perspectives in medicine · 2020Review
- Cystathionine γ-lyase deficiency enhances airway reactivity and viral-induced disease in mice exposed to side-stream tobacco smoke.Pediatric research · 2019Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe length of time for cigarette smoke (CS) exposure to cause emphysema in mice is drastically reduced when CS exposure is combined with viral infection. However, the extent of inflammatory responses and lung pathologies of mice exposed to CS and infected with influenza A virus (IAV), respiratory syncytial virus (RSV), or treated with the viral derivative dsRNA (polyinosine-polycytidylic acid [poly (I:C)] have not been compared.
methodsMice were exposed to CS or filtered air for 4 weeks and received a single dose of vehicle, AV, or RSV infection and extent of inflammation and emphysema was evaluated 14 d later. In another set of experiments, mice were instilled with poly (I:C) twice a week during the third and fourth weeks of CS exposure and immediately analyzed for extent of inflammation and lung pathologies.
resultsIn CS-exposed mice, inflammation was characterized mainly by macrophages, lymphocytes, and neutrophils after IAV infection, mainly by lymphocytes, and neutrophils after RSV infection, and mainly by lymphocytes and neutrophils after poly (I:C) instillations. Despite increased inflammation, extent of emphysema by poly (I:C) was very mild; but was robust and similar for both IAV and RSV infections with enhanced MMP-12 mRNA expression and TUNEL positivity. Both IAV and RSV infections increased the levels of IL-17, IL-1β, IL-12b, IL-18, IL-23a, Ccl-2, Ccl-7 mRNAs in the lungs of CS-exposed mice with IAV causing more increases than RSV.
conclusionCS-induced inflammatory responses and extent of emphysematous changes differ depending on the type of viral infection. These animal models may be useful to study the mechanisms by which different viruses exacerbate CS-induced inflammation and emphysema.
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