The chitinase-like protein YKL-40 modulates cystic fibrosis lung disease
The chitinase-like protein YKL-40 was found to be increased in patients with severe asthma and chronic obstructive pulmonary disease (COPD), two disease conditions featuring neutrophilic infiltrates. Based on these studies and a previous report indicating that neutrophils secrete YKL-40, we hypothes...
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| Hauptverfasser: | , , , , , , , , , , , , , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
September 20, 2011
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| In: |
PLOS ONE
Year: 2011, Jahrgang: 6, Heft: 9, Pages: 1-6 |
| ISSN: | 1932-6203 |
| DOI: | 10.1371/journal.pone.0024399 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1371/journal.pone.0024399 Verlag, lizenzpflichtig, Volltext: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0024399 
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| Verfasserangaben: | Andreas Hector, Michael S. D. Kormann, Ines Mack, Philipp Latzin, Carmen Casaulta, Elisabeth Kieninger, Zhe Zhou, Ali Ö Yildirim, Alexander Bohla, Nikolaus Rieber, Matthias Kappler, Barbara Koller, Ernst Eber, Olaf Eickmeier, Stefan Zielen, Oliver Eickelberg, Matthias Griese, Marcus A. Mall, Dominik Hartl |
MARC
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| 245 | 1 | 4 | |a The chitinase-like protein YKL-40 modulates cystic fibrosis lung disease |c Andreas Hector, Michael S. D. Kormann, Ines Mack, Philipp Latzin, Carmen Casaulta, Elisabeth Kieninger, Zhe Zhou, Ali Ö Yildirim, Alexander Bohla, Nikolaus Rieber, Matthias Kappler, Barbara Koller, Ernst Eber, Olaf Eickmeier, Stefan Zielen, Oliver Eickelberg, Matthias Griese, Marcus A. Mall, Dominik Hartl |
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| 520 | |a The chitinase-like protein YKL-40 was found to be increased in patients with severe asthma and chronic obstructive pulmonary disease (COPD), two disease conditions featuring neutrophilic infiltrates. Based on these studies and a previous report indicating that neutrophils secrete YKL-40, we hypothesized that YKL-40 plays a key role in cystic fibrosis (CF) lung disease, a prototypic neutrophilic disease. The aim of this study was (i) to analyze YKL-40 levels in human and murine CF lung disease and (ii) to investigate whether YKL-40 single-nucleotide polymorphisms (SNPs) modulate CF lung disease severity. YKL-40 protein levels were quantified in serum and sputum supernatants from CF patients and control individuals. Levels of the murine homologue BRP-39 were analyzed in airway fluids from CF-like βENaC-Tg mice. YKL-40SNPs were analyzed in CF patients. YKL-40 levels were increased in sputum supernatants and in serum from CF patients compared to healthy control individuals. Within CF patients, YKL-40 levels were higher in sputum than in serum. BRP-39 levels were increased in airways fluids from βENaC-Tg mice compared to wild-type littermates. In both CF patients and βENaC-Tg mice, YKL-40/BRP-39 airway levels correlated with the severity of pulmonary obstruction. Two YKL-40 SNPs (rs871799 and rs880633) were found to modulate age-adjusted lung function in CF patients. YKL-40/BRP-39 levelsare increased in human and murine CF airway fluids, correlate with pulmonary function and modulate CF lung disease severity genetically. These findings suggest YKL-40 as a potential biomarker in CF lung disease. | ||
| 650 | 4 | |a Asthma | |
| 650 | 4 | |a Cystic fibrosis | |
| 650 | 4 | |a Inflammatory diseases | |
| 650 | 4 | |a Mouse models | |
| 650 | 4 | |a Pulmonary function | |
| 650 | 4 | |a Serum proteins | |
| 650 | 4 | |a Single nucleotide polymorphisms | |
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