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    Airway Bacteria Quantification Using Polymerase Chain Reaction Combined with Neutrophil and Eosinophil Counts Identifies Distinct COPD Endotypes

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    Authors
    Beech, Augusta; orcid: 0000-0002-2690-5364; email: augusta.beech@manchester.ac.uk
    Lea, Simon; orcid: 0000-0003-3700-1886; email: Simon.lea@manchester.ac.uk
    Li, Jian; email: Jian.Li@manchester.ac.uk
    Jackson, Natalie; email: njackson@meu.org.uk
    Mulvanny, Alex; email: amulvanny@meu.org.uk
    Singh, Dave; email: dsingh@meu.org.uk
    Publication Date
    2021-09-27
    
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    Abstract
    Background: Chronic obstructive pulmonary disease (COPD) inflammatory endotypes are associated with different airway microbiomes. We used quantitative polymerase chain reaction (qPCR) analysis of sputum samples to establish the bacterial load upper limit in healthy controls; these values determined the bacterial colonisation prevalence in a longitudinal COPD cohort. Bacteriology combined with sputum inflammatory cells counts were used to investigate COPD endotypes. Methods: Sixty COPD patients and 15 healthy non-smoking controls were recruited. Sputum was analysed by qPCR (for Haemophilus influenzae, Moraxella catarrhalis, Streptococcus pneumoniae and Psuedomonas aeruginosa) and sputum differential cell counts at baseline and 6 months. Results: At baseline and 6 months, 23.1% and 25.6% of COPD patients were colonised with H. influenzae, while colonisation with other bacterial species was less common, e.g., S. pneumoniae—1.9% and 5.1%, respectively. H. influenzae + ve patients had higher neutrophil counts at baseline (90.1% vs. 67.3%, p 0.01), with similar results at 6 months. COPD patients with sputum eosinophil counts ≥3% at ≥1 visit rarely showed bacterial colonisation. Conclusions: The prevalence of H. influenzae colonisation was approximately 25%, with low colonisation for other bacterial species. H. influenzae colonisation was associated with sputum neutrophilia, while eosinophilic inflammation and H. influenzae colonisation rarely coexisted.
    Citation
    Biomedicines, volume 9, issue 10, page e1337
    Publisher
    MDPI
    URI
    http://hdl.handle.net/10034/625980
    Type
    article
    Description
    From MDPI via Jisc Publications Router
    History: accepted 2021-09-22, pub-electronic 2021-09-27
    Publication status: Published
    Funder: AstraZeneca; Grant(s): ESR-16-11869
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