The role of Th17 in the pathogenesis of airway remodeling
Date Issued
2010
Date
2010
Author(s)
Kuo, Jui-Mei
Abstract
Asthma is characterized by chronic allergic airway inflammation with remodeling, cell infiltration in lung, and airway hyper-responsiveness (AHR) to stimulations. Airway remodeling is structural changes of asthmatic airway, featured by increased fibrosis, epithelial hyperplasia, myocyte hyperplasia, and increased mucus secretion. Th17 cell is a kind of T helper cells with the ability to secrete IL-17 family cytokines and regulate immune responses and various kinds of inflammation, including airway remodeling. However, the role of Th17 in airway remodeling remains unknown. Here we established an OVA- sensitized animal model of asthmatic airway remodeling to investigate the role of Th17 in the progressing of airway remodel. By sacrificing the mice at different time points and simultaneously evaluated the AHR, we collected lung, for H & E and PAS staining, to display the remodeling progress of asthmatic airway, and for quantitative real-time PCR, to show the expression time and level of Th17-related factors (IL-17A, Rorc, IL-6, and IL-23R). Aligning with the results of Th17-related cytokines profile in bronchial alveolar lavage fluid (BALF), we hope to dissect the role of Th17 in the pathogenesis of airway remodeling. The results showed that an early expression of Th17-related factors in the process of the disease. Although there is no significant differences of TGF-β1 at different time points, the expression pattern of TGF-β1 in BALF align with the expression trend of Th17-related factors. Compared to histochemical staining, the existences of Th17-related factors seem to be closely followed by the subsequent progression of airway remodeling, enhanced cell infiltration, and thickening of airway wall. Although more studies are needed, Th17 might be involved in the process to trigger airway remodeling and other relative pathological changes.
Subjects
asthma
airway remodeling
type 17 T helper cell
Type
thesis
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