Lack of IL-1 receptor signaling reduces spontaneous airway eosinophilia in juvenile mice with muco-obstructive lung disease
Previous studies demonstrated spontaneous type 2 airway inflammation with eosinophilia in juvenile Scnn1b (sodium channel, non-voltage-gated 1, β-subunit)-transgenic (Scnn1b-Tg) mice with muco-obstructive lung disease. IL-1 receptor (IL-1R) signaling has been implicated in allergen-driven airway dis...
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| Hauptverfasser: | , , , , , , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
September 9, 2019
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| In: |
American journal of respiratory cell and molecular biology
Year: 2019, Jahrgang: 62, Heft: 3, Pages: 300-309 |
| ISSN: | 1535-4989 |
| DOI: | 10.1165/rcmb.2018-0359OC |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1165/rcmb.2018-0359OC Verlag, lizenzpflichtig, Volltext: https://www.atsjournals.org/doi/10.1165/rcmb.2018-0359OC 
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| Verfasserangaben: | Ryan Brown, Michelle Paulsen, Simone Schmidt, Jolanthe Schatterny, Angela Frank, Stephanie Hirtz, Rebecca Delaney, Declan Doherty, Matthias Hagner, Cliff Taggart, Sinéad Weldon, and Marcus A. Mall |
MARC
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| 520 | |a Previous studies demonstrated spontaneous type 2 airway inflammation with eosinophilia in juvenile Scnn1b (sodium channel, non-voltage-gated 1, β-subunit)-transgenic (Scnn1b-Tg) mice with muco-obstructive lung disease. IL-1 receptor (IL-1R) signaling has been implicated in allergen-driven airway disease; however, its role in eosinophilic inflammation in muco-obstructive lung disease remains unknown. In this study, we examined the role of IL-1R signaling in the development of airway eosinophilia and type 2 inflammation in juvenile Scnn1b-Tg mice. We determined effects of genetic deletion of Il1r1 (IL-1 receptor type I) on eosinophil counts, transcript levels of key type 2 cytokines, markers of eosinophil activation and apoptosis, and tissue morphology in lungs of Scnn1b-Tg mice at different time points during neonatal development. Furthermore, we measured endothelial surface expression of intercellular adhesion molecule 1 (ICAM-1), an integrin involved in eosinophil transendothelial migration, and determined effects of eosinophil depletion using an anti-IL-5 antibody on lung morphology. Lack of IL-1R reduced airway eosinophilia and structural lung damage, but it did not reduce concentrations of type 2 cytokines and associated eosinophil activation in Scnn1b-Tg mice. Structural lung damage in Scnn1b-Tg mice was also reduced by eosinophil depletion. Lack of IL-1R was associated with reduced expression of ICAM-1 on lung endothelial cells and reduced eosinophil counts in lungs from Scnn1b-Tg mice. We conclude that IL-1R signaling is implicated in airway eosinophilia independent of type 2 cytokines in juvenile Scnn1b-Tg mice. Our data suggest that IL-1R signaling may be relevant in the pathogenesis of eosinophilic airway inflammation in muco-obstructive lung diseases, which may be mediated in part by ICAM-1-dependent transmigration of eosinophils into the lungs. | ||
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