Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.718752
Title: Exploring the interplay between airway bacteria, airway inflammation, lung structure and skeletal muscle dysfunction in COPD
Author: Barker, Bethan Louise
Awarding Body: University of Leicester
Current Institution: University of Leicester
Date of Award: 2017
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Abstract:
Airway bacteria, airway inflammation, lung structure and skeletal muscle dysfunction are all recognised as important components of chronic obstructive pulmonary disease (COPD), yet the interplay between these components is not well understood. Within this thesis I present an observational study exploring relationships between airway inflammation and molecular measures of potentially pathogenic bacteria. I have shown that airway bacterial detection is associated with increased airway inflammation in stable COPD, and that this association appears to be driven by Haemophilus influenzae. I then present a cross-sectional and longitudinal study using dual energy x-ray absorptiometry measurements of body composition and have shown that airway bacterial load and inflammation are independent of body composition changes, and that loss of skeletal muscle is not associated with accelerated airway inflammation or lung function decline. Within a multi-centre exacerbation cohort study I have shown that sputum bacterial load is only weakly associated with quadriceps muscle strength in stable COPD. In addition I have shown only a small, short-lived reduction in quadriceps strength at exacerbation, suggesting that community managed exacerbations may have limited impact on long term decline in muscle and physical function in COPD patients. Finally, I present the results of a single centre study that has shown that air trapping measured using quantitative computed tomography (QCT) makes the strongest unique contribution to airflow obstruction in COPD. Moreover, H. influenzae bacterial load is related to QCT measured small airways disease, and this association is independent of the amount of neutrophilic airways inflammation. In summary, within this thesis I provide data demonstrating significant relationships between H. influenzae, airway inflammation and lung structural changes in COPD. By contrast, my findings suggest that inflammation, and in particular overspill of pulmonary inflammation is not a key pathophysiological mechanism leading to skeletal muscle depletion or dysfunction in COPD.
Supervisor: Brightling, Christopher ; Steiner, Michael Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.718752  DOI: Not available
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