Expression of epidermal growth factor receptor(EGFR) and transforming growth factor β1(TGF β1) in airway mucosa of toluene diisocyanate(TDI)-induced asthma patients

Abstract

Background and Objective: Epidermal growth factor receptor (EGFR) and TGF β1 have been known as a central regulator in airway remodeling. There have been some reports demonstrating expression of EGFR and TGF β1 in airway mucosa of asthmatic patients. However, the expression of EGFR and TGF β1 in bronchial epithelium of TDI-induced asthmatic has not been observed. The aim of this study was to observe expression of EGFR and TGF β1 and evaluate their roles in pathogenic mechanism of TDI-induced asthma. Methods: EGFR and TGF β1 expression were compared using immunohistochemistry technique in bronchial mucosa from 22 subjects with TDI-induced asthma (group Ⅰ: 10 newly diagnosed, group Ⅱ: 12 TDI-induced asthma patients with persistent asthma symptoms for more than 5 years after diagnosis), 7 non-asthmatics undergoing pneumonectomy from lung tumor, and 3 healthy subjects. The intensity of expression was analyzed by two observers. The grade of intensity was presented from 0 to 3. Subepithelial basement membrane (SBM) thickness was measured using an image analyzer. Results: EGFR expression was significantly higher in asthmatic patients than in wntrois (p>0.05), while no significant difference were nosed in TGF β1 expression (p>0.05). There was no significant difference in EGFR expression between group Ⅰ and Ⅱ (p>0.05). However, grade of TGF β1 expression was significantly higher in group Ⅱ than those of group Ⅰ (p<0.05). There was a significant difference in EGFR/TGF β1 ratio between group Ⅰ and Ⅱ (2.31±0.27 vs 1.28±0.11, p<0.05). SBM thickness of TDI-induced asthma was significantly higher than those of non-asthmatics (p<0.05), while there was no significant difference between Ⅰ and Ⅱ (p>0.05). Conclusion: These findings suggest that EGFR and TGF β1 may contribute to pathogenesis of TDI-induced asthma. However, further studies are required to evaluate the role of EGFR and TGF β1 in the pathogenesis of TDI-induced asthma.