TY - JOUR T1 - LSC 2014 abstract - Influence of a Th2 immune response on airway remodeling in asthma JF - European Respiratory Journal JO - Eur Respir J VL - 44 IS - Suppl 58 SP - 4834 AU - Katharina Dietz AU - Moritz Ulrich AU - Hoeke Baarsma AU - Kathrin Suttner AU - Melanie Königshoff AU - Carsten Schmidt-Weber AU - Ulrich Zissler Y1 - 2014/09/01 UR - http://erj.ersjournals.com/content/44/Suppl_58/4834.abstract N2 - Background: The pathological hallmarks of asthma are a Th2 driven chronic inflammation of the airways and airway remodeling. This remodeling process is known to be influenced by several signaling pathways. One of them is the Wnt signaling that is thought to be differentially regulated in asthma patients compared to healthy subjects. As a strong interaction between the epithelium and effector immune cells was previously described, it is likely that the Th2 driven asthmatic immune response is influencing the Wnt signaling in the airway epithelium.Aim: To investigate the influence of Th2 immune response on the Wnt signaling in bronchial epithelium.Methods: Bronchial epithelial cells were cultured in the presence of IL-4 and RNA was harvested after 6h and subjected to Agilent single color microarray gene expression profiling (60K). Datasets were analyzed under constant significance restrictions (p<0.05). The expression of regulated Wnt genes was validated using SYBR Green based quantitative PCR. Additionally expression of Wnt ligands in sputum supernatants of asthmatic patients versus healthy controls was determined by Western blot.Results: Significant gene expression changes of Wnt5a and FZD10 were observed in Th2-subtype specific IL-4 induced bronchial epithelial cells. The mRNA levels of both genes were significantly increased upon stimulation in comparison to a medium control (n=5). Western blot analyses suggest that Wnt5a is expressed in the sputum supernatant of asthma patients, while it is not in healthy controls.Conclusion: The results indicate that a Th2 driven immune response enhance the expression of Wnt5a by bronchial epithelial cells, which might affect the global Wnt signaling in the airway. ER -