A novel neutrophil derived inflammatory biomarker of pulmonary exacerbation in cystic fibrosis.

Hdl Handle:
http://hdl.handle.net/10147/207303
Title:
A novel neutrophil derived inflammatory biomarker of pulmonary exacerbation in cystic fibrosis.
Affiliation:
Respiratory Research Division, Department of Medicine, Royal College of Surgeons , in Ireland, Education and Research Centre, Beaumont Hospital, Dublin 9, Ireland.
Citation:
J Cyst Fibros. 2011 Oct 27.
Journal:
Journal of cystic fibrosis : official journal of the European Cystic Fibrosis, Society
Issue Date:
1-Feb-2012
URI:
http://hdl.handle.net/10147/207303
DOI:
10.1016/j.jcf.2011.09.010
PubMed ID:
22035905
Abstract:
BACKGROUND: The focus of this study was to characterize a novel biomarker for cystic fibrosis (CF) that could reflect exacerbations of the disease and could be useful for therapeutic stratification of patients, or for testing of potential drug treatments. This study focused exclusively on a protein complex containing alpha-1 antitrypsin and CD16b (AAT:CD16b) which is released into the bloodstream from membranes of pro-inflammatory primed neutrophils. METHODS: Neutrophil membrane expression and extracellular levels of AAT and CD16b were quantified by flow cytometry, Western blot analysis and by 2D-PAGE. Interleukin-8 (IL-8), tumor necrosis factor-alpha (TNF-alpha) and AAT:CD16b complex were quantified in CF plasma (n=38), samples post antibiotic treatment for 14days (n=10), chronic obstructive pulmonary disease (n=10), AAT deficient (n=10) and healthy control (n=14) plasma samples by ELISA. RESULTS: Cell priming with IL-8 and TNF-alpha caused release of the AAT:CD16b complex from the neutrophil cell membrane. Circulating plasma levels of IL-8, TNF-alpha and AAT:CD16b complex were significantly higher in patients with CF than in the other patient groups or healthy controls (P<0.05). Antibiotic treatment of pulmonary exacerbation in patients with CF led to decreased plasma protein concentrations of AAT:CD16b complex with a significant correlation with improved FEV1 (r=0.81, P=0.003). CONCLUSION: The results of this study have shown that levels of AAT:CD16b complex present in plasma correlate to the inflammatory status of patients. The AAT:CD16b biomarker may become a useful addition to the clinical diagnosis of exacerbations in CF.
Language:
ENG
ISSN:
1873-5010 (Electronic); 1569-1993 (Linking)

Full metadata record

DC FieldValue Language
dc.date.accessioned2012-02-01T10:04:23Z-
dc.date.available2012-02-01T10:04:23Z-
dc.date.issued2012-02-01T10:04:23Z-
dc.identifier.citationJ Cyst Fibros. 2011 Oct 27.en_GB
dc.identifier.issn1873-5010 (Electronic)en_GB
dc.identifier.issn1569-1993 (Linking)en_GB
dc.identifier.pmid22035905en_GB
dc.identifier.doi10.1016/j.jcf.2011.09.010en_GB
dc.identifier.urihttp://hdl.handle.net/10147/207303-
dc.description.abstractBACKGROUND: The focus of this study was to characterize a novel biomarker for cystic fibrosis (CF) that could reflect exacerbations of the disease and could be useful for therapeutic stratification of patients, or for testing of potential drug treatments. This study focused exclusively on a protein complex containing alpha-1 antitrypsin and CD16b (AAT:CD16b) which is released into the bloodstream from membranes of pro-inflammatory primed neutrophils. METHODS: Neutrophil membrane expression and extracellular levels of AAT and CD16b were quantified by flow cytometry, Western blot analysis and by 2D-PAGE. Interleukin-8 (IL-8), tumor necrosis factor-alpha (TNF-alpha) and AAT:CD16b complex were quantified in CF plasma (n=38), samples post antibiotic treatment for 14days (n=10), chronic obstructive pulmonary disease (n=10), AAT deficient (n=10) and healthy control (n=14) plasma samples by ELISA. RESULTS: Cell priming with IL-8 and TNF-alpha caused release of the AAT:CD16b complex from the neutrophil cell membrane. Circulating plasma levels of IL-8, TNF-alpha and AAT:CD16b complex were significantly higher in patients with CF than in the other patient groups or healthy controls (P<0.05). Antibiotic treatment of pulmonary exacerbation in patients with CF led to decreased plasma protein concentrations of AAT:CD16b complex with a significant correlation with improved FEV1 (r=0.81, P=0.003). CONCLUSION: The results of this study have shown that levels of AAT:CD16b complex present in plasma correlate to the inflammatory status of patients. The AAT:CD16b biomarker may become a useful addition to the clinical diagnosis of exacerbations in CF.en_GB
dc.language.isoENGen_GB
dc.titleA novel neutrophil derived inflammatory biomarker of pulmonary exacerbation in cystic fibrosis.en_GB
dc.contributor.departmentRespiratory Research Division, Department of Medicine, Royal College of Surgeons , in Ireland, Education and Research Centre, Beaumont Hospital, Dublin 9, Ireland.en_GB
dc.identifier.journalJournal of cystic fibrosis : official journal of the European Cystic Fibrosis, Societyen_GB
dc.description.provinceLeinster-

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