Journal Title
Title of Journal: Lung
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Publisher
Springer-Verlag
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Authors: K Andersson E B Shebani N Makeeva G M Roomans Z Servetnyk
Publish Date: 2010/01/16
Volume: 188, Issue: 3, Pages: 209-216
Abstract
Our primary objective was to investigate the possible contribution of controller medications to asthmatic airway remodeling by 1 comparing the apoptotic and necrotic effects of several corticosteroids and montelukast on cultured airway human bronchial surface epithelial 16HBE and submucosal Calu3 cells 2 measuring epithelial shedding potential and desmosome length in response to a cytokine challenge with or without coadministered corticosteroids and 3 studying corticosteroids and montelukast effects on intercellular adhesion molecule ICAM expression in both 16HBE and human umbilical vein endothelial cells HUVEC For this purpose apoptosis necrosis and ICAM expression were quantified by flow cytometry with 16HBE cells sensitive to both the apoptotic and necrotic effects of dexamethasone and montelukast Calu3 cells sensitive only to budesonide Transmission electron microscopy revealed decreased desmosome length in the presence of cytokines TNFα and INFγ with corticosteroids counteracting this reduction Dexamethasone beclomethasone and montelukast decreased versus increased ICAM1 expression in airway epithelial cells and HUVEC respectively For conclusions bronchial surface epithelial and submucosal cells exhibit a different sensitivity profile toward dexamethasone budesonide and montelukast with corticosteroids preventing cytokineinduced desmosomal damage in 16HBE cells The studied drugs led to increased ICAM1 expression in endothelium potentially facilitating inflammatory cell migration into lung tissue
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