ArticleAmerican journal of physiology. Lung cellular and molecular physiology2014
Cigarette smoke attenuates the RIG-I-initiated innate antiviral response to influenza infection in two murine models.
Article in American journal of physiology. Lung cellular and molecular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- Maternal Cigarette Smoke Exposure Does Not Impair Influenza Vaccine Responsiveness in Murine Offspring.Vaccines · 2025Article
- Pirfenidone Mitigates Transforming Growth Factor-β-induced Inflammation after Viral Infection.American journal of respiratory cell and molecular biology · 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
- Lactobacillus rhamnosus Restores Antiviral Signaling and Attenuates Cytokines Secretion from Human Bronchial Epithelial Cells Exposed to Cigarette Smoke and Infected with SARS-CoV-2.Probiotics and antimicrobial proteins · 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
- Early IFN-β administration protects cigarette smoke exposed mice against lethal influenza virus infection without increasing lung inflammation.Scientific reports · 2022Article
- Effects of Cigarette Smoking on Influenza Virus/Host Interplay.Pathogens (Basel, Switzerland) · 2021Review
- Long-term cigarette smoke exposure dysregulates pulmonary T cell response and IFN-γ protection to influenza virus in mouse.Respiratory research · 2021Article
- Exposure to Cigarette Smoke Enhances Pneumococcal Transmission Among Littermates in an Infant Mouse Model.Frontiers in cellular and infection microbiology · 2021Article
- Respiratory virus-associated infections in HIV-infected adults admitted to the intensive care unit for acute respiratory failure: a 6-year bicenter retrospective study (Annals of intensive care · 2020Article
- Involvement of Interferon Regulatory Factor 7 in Nicotine's Suppression of Antiviral Immune Responses.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2019Article
- Self-DNA release and STING-dependent sensing drives inflammation to cigarette smoke in mice.Scientific reports · 2019Article
- Protective role of γδ T cells in cigarette smoke and influenza infection.Mucosal immunology · 2018Article
- RIG-I overexpression decreases mortality of cigarette smoke exposed mice during influenza A virus infection.Respiratory research · 2017Article
- Interferon-λs: Front-Line Guardians of Immunity and Homeostasis in the Respiratory Tract.Frontiers in immunology · 2017Review
- Cigarette smoke represses the innate immune response to asbestos.Physiological reports · 2015Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Cigarette smoke (CS) exposure increases the frequency and severity of respiratory tract infections. Despite this association, the mechanisms underlying the increased susceptibility to respiratory virus infection are poorly understood. Retinoic acid-inducible gene I (RIG-I) is an important regulator of influenza virus-induced expression of antiviral cytokines, mainly interferons (IFNs), which are necessary to clear viral infections. In this study, we compared the innate cytokine responses of two mouse CS exposure models following a challenge with influenza A virus (IAV): 1) exposure of the mice to cigarette smoke extract (CSE) intratracheally and 2) exposure of the mice to CS in a whole body exposure chamber. Both intratracheal CSE treatment and whole body CS exposure caused antiviral immunosuppression in these mice, and both CS exposure methods inhibited RIG-I induction. CS attenuated influenza-induced antiviral IFNs and IP-10 expression in vivo. However, we did not find that CS inhibited induction of the proinflammatory cytokines IL-6 and TNF-α, whose expression was induced by IAV. Interestingly, IAV infection also increased Toll-like receptor 3 (TLR3) expression in mouse lung, but CS exposure did not impact TLR3 induction in these mice. Together, the results support our previous finding in a human lung organ culture model that the suppression of RIG-I induction and antiviral cytokine responses by CS are likely important in the enhanced susceptibility of smokers to influenza infection in the lung.
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