Publication

The cystic fibrosis neutrophil: a specialized yet potentially defective cell.

Hayes, Elaine
; 
Pohl, Kerstin
; 
McElvaney, Noel G
; 
Reeves, Emer P
Citations
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Author
Hayes, Elaine
 Pohl, Kerstin
 McElvaney, Noel G
 Reeves, Emer P
Advisors
Editors
Other Contributors
Departments
Respiratory Research Division, Department of Medicine, Education and Research, Centre, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin 9,, Ireland.
Date
2012-02-01T10:00:51Z
Date Submitted
Keywords
Other Subjects
Subject Mesh
Animals
Apoptosis
Cell Degranulation
Chemotaxis, Leukocyte
Cystic Fibrosis/genetics/*immunology/metabolism/microbiology/pathology/therapy
Humans
NADPH Oxidase/metabolism
*Neutrophil Activation
Neutrophils/*immunology/metabolism/microbiology/pathology
Phagocytosis
Respiratory Burst
Planned Date
Start Date
Collaborators
Principal Investigators
Alternative Titles
Publisher
URI
https://hdl.handle.net/10147/207165
Abstract
Cystic fibrosis (CF) is one of the commonest genetically inherited diseases in the world. It is characterized by recurrent respiratory tract infections eventually leading to respiratory failure. One of the hallmarks of this disease is a persistent and predominantly neutrophil driven inflammation. Neutrophils provide the first line of defence by killing and digesting phagocytosed bacteria and fungi, yet despite advances in our understanding of the molecular and cellular basis of CF, there remains a paradox of why recruited CF neutrophils fail to eradicate bacterial infections in the lung. This review describes mechanisms involved in neutrophil migration, microbial killing and apoptosis leading to inflammatory resolution. We discuss dysregulated neutrophil activity and consider genetic versus inflammatory neutrophil reprogramming in CF and ultimately pharmacological modulation of the CF neutrophil for therapeutic intervention.
Language
eng
Citation
Arch Immunol Ther Exp (Warsz). 2011 Apr;59(2):97-112. Epub 2011 Feb 11.
ISSN
1661-4917 (Electronic)
0004-069X (Linking)
eISSN
ISBN
DOI
10.1007/s00005-011-0113-6
PMID
21311988
PMCID
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Funding Sources
Funding Amounts
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