Exacerbation status is linked to dysfunctional phagocytosis in stable in Chronic Obstructive Pulmonary Disease (COPD) patients but not to pulmonary function
Journal Contribution ResearchOnline@JCUAbstract
Introduction/Aim: Chronic obstructive pulmonary disease (COPD) is a significant and increasing public health challenge. Much of the disease burden and economic cost of COPD is associated with acute exacerbations and resulting bacterial colonisation of the airways. The aim of this study is to determine whether the bactericidal functions of phagocytic cells (monocytes and neutrophils) are impaired, predisposing COPD patients to increased bacterial infections. Method: Spirometry and venous blood were collected from COPD patients across the GOLD2015 spectrum and a group of healthy controls were recruited for comparison. Flow cytometry was used to determine differential counts for a range of leukocytes and internalisation of fluorescently labelled Streptococcus pneumoniae in whole blood phagocytes. Groups were compared by ANOVA and post hoc tests. Results: Results demonstrated that peripheral blood monocytes (p=0.04) and neutrophils (p=<0.0005) in exacerbation prone COPD patients had significant reductions in both bactericidal activity against S. pneumoniae (p=0.01) and internalisation of inert microparticles (p=0.01) compared to healthy controls and also stable COPD patients. Data collection remains ongoing. Conclusion: This study has demonstrated that defective phagocytosis in COPD patients prone to exacerbations is irrespective of disease severity (according to GOLD2015). Thus dysfunctional cellular activity of blood monocytes and neutrophils, and a failure to mount an appropriate immune response to infection, may enable bacteria to overwhelm host defences leading to further lung tissue damage.
Journal
Respirology
Publication Name
N/A
Volume
23
ISBN/ISSN
1440-1843
Edition
N/A
Issue
Suppl 1
Pages Count
1
Location
Brisbane
Publisher
Wiley-Blackwell
Publisher Url
N/A
Publisher Location
Respirology
Publish Date
N/A
Url
N/A
Date
N/A
EISSN
N/A
DOI
10.1111/resp.13268