Expression of epidermal growth factor receptor (EGFR) and transforming growth factor beta1 (TGF beta1) in airway mucosa of toluene diisocyanate (TDI)-induced asthma patients.
- Author:
Ik Soo CHOI
1
;
Soo Keol LEE
;
Yu Jin SUH
;
Jeong Hee CHOI
;
Hae Sim PARK
;
Sun Sin KIM
;
Young Mok LEE
;
Doo Kyung YANG
;
Choon Sik PARK
Author Information
1. Sam-Seon Hospital, Korea.
- Publication Type:Original Article
- Keywords:
EGFR;
TGF 1;
airway remodeling;
TDI-induced asthma
- MeSH:
Airway Remodeling;
Asthma*;
Basement Membrane;
Epidermal Growth Factor*;
Epithelium;
Humans;
Immunohistochemistry;
Lung;
Mucous Membrane*;
Nose;
Pneumonectomy;
Receptor, Epidermal Growth Factor*;
Toluene 2,4-Diisocyanate*;
Toluene*;
Transforming Growth Factor beta1*;
Transforming Growth Factors*
- From:Journal of Asthma, Allergy and Clinical Immunology
2002;22(3):567-576
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND AND OBJECTIVE: Epidermal growth factor receptor(EGFR) and TGF beta1 have been known as a central regulator in airway remodeling. There have been some reports demonstrating expression of EGFR and TGF beta1 in airway mucosa of asthmatic patients. However, the expression of EGFR and TGF beta1 in bronchial epithelium of TDI-induced asthmatics has not been observed. The aim of this study was to observe expression of EGFR and TGF beta1 and evaluate their roles in pathogenic mechanism of TDI-induced asthma. METHODS: EGFR and TGF beta1 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 beta1 expression (p>0.05). There was no significant difference in EGFR expression between group I and II (p>0.05). However, grade of TGF beta1 expression was significantly higher in group II than those of group I (p<0.05). There was a significant difference in EGFR/TGF beta1 ratio between 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 group I and II (p>0.05). CONCLUSION: These findings suggest that EGFR and TGF beta1 may contribute to pathogenesis of TDI-induced asthma. However, further studies are required to evaluate the role of EGFR and TGF beta1 in the pathogenesis of TDI-induced asthma.
