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Mediators of Inflammation
Volume 2015, Article ID 408935, 11 pages
Research Article

Free DNA in Cystic Fibrosis Airway Fluids Correlates with Airflow Obstruction

1Department of Pediatric Pulmonology, Hauner Children’s Hospital, Ludwig Maximilians University, The German Center for Lung Research (DZL), 80377 Munich, Germany
2Department of Translational Pulmonology, Translational Lung Research Center Heidelberg (TLRC), University of Heidelberg, The German Center for Lung Research (DZL), 69120 Heidelberg, Germany
3Comprehensive Pneumology Center, Institute of Lung Biology and Disease (iLBD), University Hospital, Ludwig Maximilians University and Helmholtz Zentrum München, The German Center for Lung Research (DZL), 81377 Munich, Germany
4Children’s Hospital and Interdisciplinary Center for Infectious Diseases, University of Tübingen, 72076 Tübingen, Germany
5Department of Operative Dentistry & Periodontology, Saarland University, 66424 Homburg, Germany
6Biomedical Ultrastructure Research Lab, Division of Animal Structure and Function, Department of Cell Biology, University of Salzburg, 5020 Salzburg, Austria

Received 11 January 2015; Revised 11 March 2015; Accepted 13 March 2015

Academic Editor: Pham My-Chan Dang

Copyright © 2015 Veronica Marcos et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Chronic obstructive lung disease determines morbidity and mortality of patients with cystic fibrosis (CF). CF airways are characterized by a nonresolving neutrophilic inflammation. After pathogen contact or prolonged activation, neutrophils release DNA fibres decorated with antimicrobial proteins, forming neutrophil extracellular traps (NETs). NETs have been described to act in a beneficial way for innate host defense by bactericidal, fungicidal, and virucidal actions. On the other hand, excessive NET formation has been linked to the pathogenesis of autoinflammatory and autoimmune disease conditions. We quantified free DNA structures characteristic of NETs in airway fluids of CF patients and a mouse model with CF-like lung disease. Free DNA levels correlated with airflow obstruction, fungal colonization, and CXC chemokine levels in CF patients and CF-like mice. When viewed in combination, our results demonstrate that neutrophilic inflammation in CF airways is associated with abundant free DNA characteristic for NETosis, and suggest that free DNA may be implicated in lung function decline in patients with CF.