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Title: Electronic-Cigarette Use Alters Nasal Mucosal Immune Response to Live-attenuated Influenza Virus. A Clinical Trial.

Authors: Rebuli, Meghan E; Glista-Baker, Ellen; Hoffman, Jessica R; Duffney, Parker F; Robinette, Carole; Speen, Adam M; Pawlak, Erica A; Dhingra, Radhika; Noah, Terry L; Jaspers, Ilona

Published In Am J Respir Cell Mol Biol, (2021 01)

Abstract: Inhalation of tobacco smoke has been linked to increased risk of viral infection, such as influenza. Inhalation of electronic-cigarette (e-cigarette) aerosol has also recently been linked to immune suppression within the respiratory tract, specifically the nasal mucosa. We propose that changes in the nasal mucosal immune response modify antiviral host-defense responses in e-cigarette users. Nonsmokers, cigarette smokers, and e-cigarette users were inoculated with live-attenuated influenza virus (LAIV) to safely examine the innate immune response to influenza infection. Before and after LAIV inoculation, we collected nasal epithelial-lining fluid, nasal lavage fluid, nasal-scrape biopsy specimens, urine, and blood. Endpoints examined include cytokines and chemokines, influenza-specific IgA, immune-gene expression, and markers of viral load. Statistical analysis included primary comparisons of cigarette and e-cigarette groups with nonsmokers, as well as secondary analysis of demographic factors as potential modifiers. Markers of viral load did not differ among the three groups. Nasal-lavage-fluid anti-LAIV IgA levels increased in nonsmokers after LAIV inoculation but did not increase in e-cigarette users and cigarette smokers. LAIV-induced gene-expression changes in nasal biopsy specimens differed in cigarette smokers and e-cigarette users as compared with nonsmokers, with a greater number of genes changed in e-cigarette users, mostly resulting in decreased expression. The top downregulated genes in cigarette smokers were SMPD3, NOS2A, and KLRB1, and the top downregulated genes in e-cigarette users were MR1, NT5E, and HRAS. Similarly, LAIV-induced cytokine levels in nasal epithelial-lining fluid differed among the three groups, including decreased antiviral host-defense mediators (IFNγ, IL6, and IL12p40). We also detected that sex interacted with tobacco-product exposure to modify LAIV-induced immune-gene expression. Our results demonstrate that e-cigarette use altered nasal LAIV-induced immune responses, including gene expression, cytokine and chemokine release, and LAIV-specific IgA levels. Together, these data suggest that e-cigarette use induces changes in the nasal mucosa that are consistent with the potential for altered respiratory antiviral host-defense function.Clinical trial registered with www.clinicaltrials.gov (NCT02019745).

PubMed ID: 33095645 Exiting the NIEHS site

MeSH Terms: Adult; Cytokines/immunology; Female; Humans; Immunity, Innate/drug effects; Immunity, Innate/immunology; Immunity, Mucosal/drug effects*; Immunity, Mucosal/immunology; Inflammation/immunology; Inflammation/virology; Influenza Vaccines/immunology*; Influenza, Human/immunology; Influenza, Human/virology; Male; Nasal Lavage Fluid/immunology; Nasal Lavage Fluid/virology; Nasal Mucosa/drug effects*; Nasal Mucosa/immunology; Smoke/adverse effects; Tobacco Products/adverse effects*; Vaccines, Attenuated/immunology*; Vaping/adverse effects*; Vaping/immunology*; Young Adult

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