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COVID-19 and COPD: a narrative review of the basic science and clinical outcomes

Andrew Higham, Alexander Mathioudakis, Jørgen Vestbo, Dave Singh
European Respiratory Review 2020 29: 200199; DOI: 10.1183/16000617.0199-2020
Andrew Higham
1Division of Infection, Immunity and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, The University of Manchester and Manchester University NHS Foundation Trust, Manchester, UK
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  • For correspondence: Andrew.Higham@manchester.ac.uk
Alexander Mathioudakis
1Division of Infection, Immunity and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, The University of Manchester and Manchester University NHS Foundation Trust, Manchester, UK
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Jørgen Vestbo
1Division of Infection, Immunity and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, The University of Manchester and Manchester University NHS Foundation Trust, Manchester, UK
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Dave Singh
1Division of Infection, Immunity and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, The University of Manchester and Manchester University NHS Foundation Trust, Manchester, UK
2Medicines Evaluation Unit, Manchester, UK
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  • FIGURE 1
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    FIGURE 1

    The implications of angiotensin converting enzyme (ACE)2 dysfunction during severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection. In the absence of infection, ACE2 is working at capacity and the levels of angiotensin II (ang II) are tightly regulated by conversion to angiotensin 1–7 (ang 1–7). Ang 1–7 activates the Mas receptor to regulate inflammation and vasomotor tone. During SARS-CoV-2 infection, ACE2 activity is reduced due to receptor occupancy, shedding and internalisation and the levels of ang II increase. Ang II activates the AT1 receptor to cause increased pro-inflammatory cytokine production, increased vasoconstriction, increased vascular permeability, oedema and lung injury. Pulmonary inflammation increases and acute severe respiratory failure may ensue.

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    FIGURE 2

    Inhaled corticosteroid (ICS) use in COPD: implications for coronavirus disease 2019. ICS prevent exacerbations in eosinophilic COPD patients, probably in part by targeting type 2 inflammation in these individuals. ICS may have further benefit by reducing the ability of severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) to proliferate, and by limiting SARS-CoV-2 cellular entry by reducing angiotensin converting enzyme (ACE)2 expression as a result of inhibiting type 1 interferon (IFN) production. However, immunosuppression may increase susceptibility to respiratory infections leading to secondary bacterial colonisation and increasing the risk for pneumonia in some individuals. #: ICS reduces ACE2 expression by reducing type 1 IFN production.

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    FIGURE 3

    Prevalence of COPD among patients with coronavirus disease 2019 with different severity. Data summary from larger patient cohorts (n >1000 for hospitalised patients or >500 for critically ill patients).

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    FIGURE 4

    Impact of COPD on the outcomes of coronavirus disease 2019. Data summary from larger patient cohorts (n >1000 for hospitalised patients or >500 for critically ill patients). ICU: intensive care unit.

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    FIGURE 5

    The key issues addressed by this review. SARS-CoV-2: severe acute respiratory syndrome-coronavirus-2; COVID-19: coronavirus disease 2019; ICS: inhaled corticosteroids; ACE2: angiotensin converting enzyme 2. +: benefits of ICS; −: dangers of ICS.

Tables

  • Figures
  • TABLE 1

    Expression of genes/proteins related to severe acute respiratory syndrome-coronavirus-2 infection in controls# and COPD patients

    First author [ref.]Key findingsSample typePatient groups
    ACE2FurinTMPRSS2
    Cai [40]↑↑No differenceBronchial epitheliumCurrent smoker versus never-smoker
    COPD versus ex-smoker
    Leung [28]↑Not quantifiedNot quantifiedBronchial epitheliumCurrent smoker versus never-smoker
    COPD versus controls
    Negative correlation with FEV1 %
    Smith [41]↑Not quantifiedNo differenceWhole lung tissueCurrent smoker versus never-smoker
    COPD versus current smoker
    Brake [27]↑Not quantifiedNot quantifiedBronchial epitheliumCOPD versus controls¶
    Zhang [29]↑No difference↑Bronchial epitheliumCurrent smoker versus never-smoker
    Radzikowska [42]↑Not quantifiedNot quantifiedBronchial biopsyCurrent smoker versus never-smoker
    Higham [43]↑No difference¶No differenceBronchial epitheliumNegative correlation with FEV1 %
    Overweight COPD versus not overweight COPD

    ↑: increase in cell number; FEV1: forced expiratory volume in 1 s. #: controls were a mixture of never-, ex- and current smokers; ¶: data not presented in manuscript.

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    COVID-19 and COPD: a narrative review of the basic science and clinical outcomes
    Andrew Higham, Alexander Mathioudakis, Jørgen Vestbo, Dave Singh
    European Respiratory Review Dec 2020, 29 (158) 200199; DOI: 10.1183/16000617.0199-2020

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    COVID-19 and COPD: a narrative review of the basic science and clinical outcomes
    Andrew Higham, Alexander Mathioudakis, Jørgen Vestbo, Dave Singh
    European Respiratory Review Dec 2020, 29 (158) 200199; DOI: 10.1183/16000617.0199-2020
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    • Article
      • Abstract
      • Abstract
      • Introduction
      • Mechanisms of susceptibility to SARS-CoV-2 infection in COPD patients
      • ICS use in COPD: implications for COVID-19
      • Epidemiology and clinical outcomes of COVID-19 in COPD patients
      • Clinical and research implications
      • Conclusion
      • Footnotes
      • References
    • Figures & Data
    • Info & Metrics
    • PDF

    Subjects

    • Respiratory infections and tuberculosis
    • COPD and smoking
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