Bronchial mucosal inflammation and illness severity in response to experimental rhinovirus infection in COPD - 05/10/20
Abstract |
Background |
Respiratory viral infection causes chronic obstructive pulmonary disease (COPD) exacerbations. We previously reported increased bronchial mucosa eosinophil and neutrophil inflammation in patients with COPD experiencing naturally occurring exacerbations. But it is unclear whether virus per se induces bronchial mucosal inflammation, nor whether this relates to exacerbation severity.
Objectives |
We sought to determine the extent and nature of bronchial mucosal inflammation following experimental rhinovirus (RV)-16–induced COPD exacerbations and its relationship to disease severity.
Methods |
Bronchial mucosal inflammatory cell phenotypes were determined at preinfection baseline and following experimental RV infection in 17 Global Initiative for Chronic Obstructive Lung Disease stage II subjects with COPD and as controls 20 smokers and 11 nonsmokers with normal lung function. No subject had a history of asthma/allergic rhinitis: all had negative results for aeroallergen skin prick tests.
Results |
RV infection increased the numbers of bronchial mucosal eosinophils and neutrophils only in COPD and CD8+ T lymphocytes in patients with COPD and nonsmokers. Monocytes/macrophages, CD4+ T lymphocytes, and CD20+ B lymphocytes were increased in all subjects. At baseline, compared with nonsmokers, subjects with COPD and smokers had increased numbers of bronchial mucosal monocytes/macrophages and CD8+ T lymphocytes but fewer numbers of CD4+ T lymphocytes and CD20+ B lymphocytes. The virus-induced inflammatory cells in patients with COPD were positively associated with virus load, illness severity, and reductions in lung function.
Conclusions |
Experimental RV infection induces bronchial mucosal eosinophilia and neutrophilia only in patients with COPD and monocytes/macrophages and lymphocytes in both patients with COPD and control subjects. The virus-induced inflammatory cell phenotypes observed in COPD positively related to virus load and illness severity. Antiviral/anti-inflammatory therapies could attenuate bronchial inflammation and ameliorate virus-induced COPD exacerbations.
Le texte complet de cet article est disponible en PDF.Key words : Rhinovirus infection, eosinophils, inflammation, chronic obstructive pulmonary disease exacerbation
Abbreviations used : COPD, Epi, RV, Sub
Plan
| This study was supported by an Academy of Medical Sciences and Wellcome Trust Starter Grant award (P.M.), a European Respiratory Society fellowship (M.C.), a Medical Research Council Clinical Research Fellowship (S.D.M.) and Medical Research Council Program Grant G0600879 (P.J.B., I.M.A., and S.L.J.), British Medical Association H.C. Roscoe Fellowships (J.F., S.D.M., and P.M.), British Lung Foundation/Severin Wunderman Family Foundation Lung Research Program Grant P00/2 (S.L.J.), Wellcome Trust Grant 083,567/Z/07/Z for the Centre for Respiratory Infection, Imperial College and the National Institute for Health Research (NIHR) Biomedical Research Centre funding scheme, and the NIHR Clinical Lecturer funding scheme; an unrestricted grant from GlaxoSmithKline; and a grant from Pfizer UK. Spirometers were provided by Micro Medical Ltd, Rochester, UK. |
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| Disclosure of potential conflict of interest: M. Contoli reports grants from Chiesi and personal fees from Chiesi, AstraZeneca, Boehringer Ingelheim, Novartis, Menarini, Mundipharma, Almirall, and Zambon outside the submitted work. A. Papi reports grants, personal fees, nonfinancial support, and other support from Chiesi, AstraZeneca, GlaxoSmithKline, Boehringer Ingelheim, and Merck Sharp & Dohme; personal fees and nonfinancial support from Menarini, Novartis, and Zambon; and grants, personal fees, nonfinancial support, and other support from Pfizer, Takeda, Mundipharma, and Teva outside the submitted work. S. L. Johnston reports board membership for Therapeutic Frontiers Ltd and Virtus Respiratory Research Ltd; consultancy fees/grants from AstraZeneca, Apollo, Bayer, Synairgen, Novartis, Boehringer Ingelheim, Chiesi, GlaxoSmithKline, and Aviragen; and patents (International Patent Application No. PCT/GB05/50031, UK Patent Application No. 0518425.4, Patent No. 7569216, European Patent No. 1734987, Hong Kong Patent No. 1097181, Japanese Patent No. 4807526, New Hong Kong Divisional Patent Application No. 11100187.0, and European Patent No. 13305152) outside the submitted work. The rest of the authors declare that they have no relevant conflicts of interest. |
Vol 146 - N° 4
P. 840 - octobre 2020 Retour au numéro
Article précédent
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