Thymic stromal lymphopoietin, but not ezrin, could be an early biomarker of airway epithelial dysfunction in acute allergic asthma

Author(s):  
Virginija Kalinauskaite-Zukauske ◽  
Andrius Januskevicius ◽  
Ieva Janulaityte ◽  
Kestutis Malakauskas
2017 ◽  
Vol 199 (1) ◽  
pp. 48-61 ◽  
Author(s):  
Carina Klaßen ◽  
Anna Karabinskaya ◽  
Lien Dejager ◽  
Sabine Vettorazzi ◽  
Justine Van Moorleghem ◽  
...  

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Rakesh K. Kumar ◽  
Jessica S. Siegle ◽  
Gerard E. Kaiko ◽  
Cristan Herbert ◽  
Joerg E. Mattes ◽  
...  

The pathogenesis of allergic asthma in childhood remains poorly understood. Environmental factors which appear to contribute to allergic sensitisation, with development of a Th2-biased immunological response in genetically predisposed individuals, include wheezing lower respiratory viral infections in early life and exposure to airborne environmental pollutants. These may activate pattern recognition receptors and/or cause oxidant injury to airway epithelial cells (AECs). In turn, this may promote Th2 polarisation via a “final common pathway” involving interaction between AEC, dendritic cells, and CD4+ T lymphocytes. Potentially important cytokines produced by AEC include thymic stromal lymphopoietin and interleukin-25. Their role is supported by in vitro studies using human AEC, as well as by experiments in animal models. To date, however, few investigations have employed models of the induction phase of childhood asthma. Further research may help to identify interventions that could reduce the risk of allergic asthma.


Allergy ◽  
2014 ◽  
Vol 69 (8) ◽  
pp. 1068-1076 ◽  
Author(s):  
A. Froidure ◽  
C. Shen ◽  
D. Gras ◽  
J. Van Snick ◽  
P. Chanez ◽  
...  

2020 ◽  
Vol 42 (12) ◽  
pp. 1399-1406
Author(s):  
Yan-Li Li ◽  
Xi-Qian Xing ◽  
Yi Xiao ◽  
Yan-Hong Liu ◽  
Yu-Shan Zhou ◽  
...  

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Rachel L. Clifford ◽  
Jamie Patel ◽  
Julia L. MacIsaac ◽  
Lisa M. McEwen ◽  
Simon R. Johnson ◽  
...  

Abstract The airway epithelium forms the interface between the inhaled environment and the lung. The airway epithelium is dysfunctional in asthma and epigenetic mechanisms are considered a contributory factor. We hypothesised that the DNA methylation profiles of cultured primary airway epithelial cells (AECs) would differ between cells isolated from individuals with asthma (n = 17) versus those without asthma (n = 16). AECs were isolated from patients by two different isolation techniques; pronase digestion (9 non-asthmatic, 8 asthmatic) and bronchial brushings (7 non-asthmatic and 9 asthmatic). DNA methylation was assessed using an Illumina Infinium HumanMethylation450 BeadChip array. DNA methylation of AECs clustered by isolation technique and linear regression identified 111 CpG sites differentially methylated between isolation techniques in healthy individuals. As a consequence, the effect of asthmatic status on DNA methylation was assessed within AEC samples isolated using the same technique. In pronase isolated AECs, 15 DNA regions were differentially methylated between asthmatics and non-asthmatics. In bronchial brush isolated AECs, 849 differentially methylated DNA regions were identified with no overlap to pronase regions. In conclusion, regardless of cell isolation technique, differential DNA methylation was associated with asthmatic status in AECs, providing further evidence for aberrant DNA methylation as a signature of epithelial dysfunction in asthma.


Sign in / Sign up

Export Citation Format

Share Document