Journal
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
Volume 142, Issue 3, Pages 815-+Publisher
MOSBY-ELSEVIER
DOI: 10.1016/j.jaci.2017.10.017
Keywords
Chronic obstructive pulmonary disease; glucose; viral infection; airway inflammation; bacterial infection
Categories
Funding
- Cystic Fibrosis Trust & British Lung Foundation (BLF) Summer Studentship [ss15-7]
- Imperial College Healthcare Trust Biomedical Research Centre Grant [P33132]
- Academy of Medical Sciences
- Wellcome Trust Starter Grant
- Imperial College Antimicrobial Resistance consortium fellowship
- Medical Research Council Program Grant [G0600879]
- British Medical Association
- BLF/Severin Wunderman Family Foundation Lung Research Program Grant [P00/2]
- Imperial College
- NIHR BRC funding scheme
- NIHR Senior Investigator Award
- NIHR Clinical Lecturer funding scheme
- MRC [G0600879] Funding Source: UKRI
- Austrian Science Fund (FWF) [P33132] Funding Source: Austrian Science Fund (FWF)
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Background: Patients with chronic obstructive pulmonary disease (COPD) have increased susceptibility to respiratory tract infection, which contributes to disease progression and mortality, but mechanisms of increased susceptibility to infection remain unclear. Objectives: The aim of this study was to determine whether glucose concentrations were increased in airway samples (nasal lavage fluid, sputum, and bronchoalveolar lavage fluid) from patients with stable COPD and to determine the effects of viral infection on sputum glucose concentrations and how airway glucose concentrations relate to bacterial infection. Methods: We measured glucose concentrations in airway samples collected from patients with stable COPD and smokers and nonsmokers with normal lung function. Glucose concentrations were measured in patients with experimentally induced COPD exacerbations, and these results were validated in patients with naturally acquired COPD exacerbations. Relationships between sputum glucose concentrations, inflammatory markers, and bacterial load were examined. Results: Sputum glucose concentrations were significantly higher in patients with stable COPD compared with those in control subjects without COPD. In both experimental virus induced and naturally acquired COPD exacerbations, sputum and nasal lavage fluid glucose concentrations were increased over baseline values. There were significant correlations between sputum glucose concentrations and sputum inflammatory markers, viral load, and bacterial load. Airway samples with higher glucose concentrations supported more Pseudomonas aeruginosa growth in vitro. Conclusions: Airway glucose concentrations are increased in patients with stable COPD and further increased during COPD exacerbations. Increased airway glucose concentrations might contribute to bacterial infections in both patients with stable and those with exacerbated COPD. This has important implications for the development of nonantibiotic therapeutic strategies for the prevention or treatment of bacterial infection in patients with COPD.
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