Expression of transforming growth factorbeta1 (TGFbeta1) and TGFbeta receptor II (R II) in airway mucosa of toluene diisocyanate (TDI)-induced asthma: relationships with persistent asthmatic symptoms.
- Author:
Soo Keol LEE
1
;
Sun Min LEE
;
Ki Baik HAHM
;
Hyun Ee YIM
;
Sun Sin KIM
;
Dong Ho NAHM
;
Hae Sim PARK
Author Information
1. Department of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon, Korea.
- Publication Type:Original Article
- Keywords:
TDI induced asthma;
TGF-beta-1;
TGF receptor II;
Asthma symptom
- MeSH:
Antibodies, Monoclonal;
Asthma*;
Endothelium, Vascular;
Enzyme-Linked Immunosorbent Assay;
Extracellular Matrix;
Humans;
Immunoglobulin E;
Immunoglobulin G;
Immunohistochemistry;
Lung;
Mucous Membrane*;
Muscle, Smooth;
Pneumonectomy;
Prognosis;
Serum Albumin;
Toluene 2,4-Diisocyanate*;
Toluene*;
Transforming Growth Factor beta*;
Transforming Growth Factor beta1
- From:Korean Journal of Medicine
2001;61(6):623-633
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: The underlying mechanism to explain the poor prognosis of TDI-induced asthma is unknown. We performed this study to evaluate the role of TGFbeta1 and its receptor, TFGbeta receptor II (RII) in TDI-induced asthma. METHODS: We applied immunohistochemistry with monoclonal antibodies to TGFbeta1 and RII in bronchial mucosa from 22 subjects with TDI-induced asthma (group I: 10 newly diagnosed, group II: 12 subjects with persistent asthma symptoms for more than 4 years after diagnosis) and 8 non-asthmatics undergoing pneumonectomy from lung tumor. The expression was analyzed in 4 areas of bronchial tissue-epithelium (EP), vascular endothelium (VE), smooth muscle (SM), mucous gland (MG). The grade of intensity was presented from 0 to 3. Subepithelial basement memberane (SBM) and submucosal extracellular matrix (SECM) thickness were measured using an image analyzer. Serum specific IgE and IgG antibody levels to TDI- human serum albumin (HSA) conjugate were detected by ELISA. RESULTS: Grade of TGFbeta1 expression was significantly higher in EP, VE and SM in group II than those of group I of TDI-induced asthma (p<0.05 respectively), with significant difference in SM only in RII expression. SBM and SECM thickness of TDI-induced asthma were significantly higher than those of non-asthmatics (p<0.05, respectively), while there was no significant difference between group I and II (p>0.05). Significant correlations were noted between asthma duration after diagonsis and intensity of TGFbeta1 expression in EP, VE and SM (p<0.05, respectively), with no significant correlations with RII expression (p>0.05). TGF 1 expression was significantly higher in EP, VE and SM in subjects with specific IgG antibody to TDI-HSA than those without it (p<0.05). CONCLUSION: These findings suggest that TGFbeta1 may contribute to develop persistent asthma symptoms in TDI-induced asthma.
