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E-cigarette vapour enhances pneumococcal adherence to airway epithelial cells.
Eur Respir J. 2018 02; 51(2)ER

Abstract

E-cigarette vapour contains free radicals with the potential to induce oxidative stress. Since oxidative stress in airway cells increases platelet-activating factor receptor (PAFR) expression, and PAFR is co-opted by pneumococci to adhere to host cells, we hypothesised that E-cigarette vapour increases pneumococcal adhesion to airway cells.Nasal epithelial PAFR was assessed in non-vaping controls, and in adults before and after 5 min of vaping. We determined the effect of vapour on oxidative stress-induced, PAFR-dependent pneumococcal adhesion to airway epithelial cells in vitro, and on pneumococcal colonisation in the mouse nasopharynx. Elemental analysis of vapour was done by mass spectrometry, and oxidative potential of vapour assessed by antioxidant depletion in vitroThere was no difference in baseline nasal epithelial PAFR expression between vapers (n=11) and controls (n=6). Vaping increased nasal PAFR expression. Nicotine-containing and nicotine-free E-cigarette vapour increased pneumococcal adhesion to airway cells in vitro Vapour-stimulated adhesion in vitro was attenuated by the PAFR blocker CV3988. Nicotine-containing E-cigarette vapour increased mouse nasal PAFR expression, and nasopharyngeal pneumococcal colonisation. Vapour contained redox-active metals, had considerable oxidative activity, and adhesion was attenuated by the antioxidant N-acetyl cysteine.This study suggests that E-cigarette vapour has the potential to increase susceptibility to pneumococcal infection.

Authors+Show Affiliations

Centre for Genomics and Child Health, Blizard Institute, Queen Mary University of London, London, UK.Centre for Genomics and Child Health, Blizard Institute, Queen Mary University of London, London, UK.The Dept of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool, Liverpool, UK.MRC-PHE Centre for Environment and Health, King's College London, London, UK. NIHR Health Protection Research Unit on Health Impacts of Environmental Hazards, King's College London, London, UK.NIHR Health Protection Research Unit on Health Impacts of Environmental Hazards, King's College London, London, UK.The Dept of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool, Liverpool, UK.Division of Pulmonology, Dept of Medicine, University of Cape Town and UCT Lung Institute, Cape Town, South Africa.The Dept of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool, Liverpool, UK.Centre for Genomics and Child Health, Blizard Institute, Queen Mary University of London, London, UK j.grigg@qmul.ac.uk.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

29437942

Citation

Miyashita, Lisa, et al. "E-cigarette Vapour Enhances Pneumococcal Adherence to Airway Epithelial Cells." The European Respiratory Journal, vol. 51, no. 2, 2018.
Miyashita L, Suri R, Dearing E, et al. E-cigarette vapour enhances pneumococcal adherence to airway epithelial cells. Eur Respir J. 2018;51(2).
Miyashita, L., Suri, R., Dearing, E., Mudway, I., Dove, R. E., Neill, D. R., Van Zyl-Smit, R., Kadioglu, A., & Grigg, J. (2018). E-cigarette vapour enhances pneumococcal adherence to airway epithelial cells. The European Respiratory Journal, 51(2). https://doi.org/10.1183/13993003.01592-2017
Miyashita L, et al. E-cigarette Vapour Enhances Pneumococcal Adherence to Airway Epithelial Cells. Eur Respir J. 2018;51(2) PubMed PMID: 29437942.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - E-cigarette vapour enhances pneumococcal adherence to airway epithelial cells. AU - Miyashita,Lisa, AU - Suri,Reetika, AU - Dearing,Emma, AU - Mudway,Ian, AU - Dove,Rosamund E, AU - Neill,Daniel R, AU - Van Zyl-Smit,Richard, AU - Kadioglu,Aras, AU - Grigg,Jonathan, Y1 - 2018/02/07/ PY - 2017/08/04/received PY - 2017/11/20/accepted PY - 2018/2/14/entrez PY - 2018/2/14/pubmed PY - 2019/4/26/medline JF - The European respiratory journal JO - Eur Respir J VL - 51 IS - 2 N2 - E-cigarette vapour contains free radicals with the potential to induce oxidative stress. Since oxidative stress in airway cells increases platelet-activating factor receptor (PAFR) expression, and PAFR is co-opted by pneumococci to adhere to host cells, we hypothesised that E-cigarette vapour increases pneumococcal adhesion to airway cells.Nasal epithelial PAFR was assessed in non-vaping controls, and in adults before and after 5 min of vaping. We determined the effect of vapour on oxidative stress-induced, PAFR-dependent pneumococcal adhesion to airway epithelial cells in vitro, and on pneumococcal colonisation in the mouse nasopharynx. Elemental analysis of vapour was done by mass spectrometry, and oxidative potential of vapour assessed by antioxidant depletion in vitroThere was no difference in baseline nasal epithelial PAFR expression between vapers (n=11) and controls (n=6). Vaping increased nasal PAFR expression. Nicotine-containing and nicotine-free E-cigarette vapour increased pneumococcal adhesion to airway cells in vitro Vapour-stimulated adhesion in vitro was attenuated by the PAFR blocker CV3988. Nicotine-containing E-cigarette vapour increased mouse nasal PAFR expression, and nasopharyngeal pneumococcal colonisation. Vapour contained redox-active metals, had considerable oxidative activity, and adhesion was attenuated by the antioxidant N-acetyl cysteine.This study suggests that E-cigarette vapour has the potential to increase susceptibility to pneumococcal infection. SN - 1399-3003 UR - https://www.unboundmedicine.com/medline/citation/29437942/E_cigarette_vapour_enhances_pneumococcal_adherence_to_airway_epithelial_cells_ DB - PRIME DP - Unbound Medicine ER -