Expression of Transforming Growth Factor-Beta in Patients with Interstitial Lung Diseases (ILD).
10.4046/trd.1996.43.2.164
- Author:
Sung Soo PARK
1
;
Kyung Sang LEE
;
Suck Chul YANG
;
Ho Joo YOON
;
Dong Ho SHIN
;
Dong Hoo LEE
;
Jung Dal LEE
;
Jung Hee LEE
Author Information
1. Department of Pulmonary Medicine, Hanyang University Hospital, Korea.
- Publication Type:Original Article
- Keywords:
Expression;
Transforming growth factor-beta;
Interstitial lung diseases
- MeSH:
Antibodies, Neutralizing;
Bleomycin;
Eosinophilic Granuloma;
Epithelial Cells;
Epithelioid Cells;
Extracellular Matrix;
Fibroblasts;
Fibrosis;
Humans;
Idiopathic Pulmonary Fibrosis;
Lung;
Lung Diseases;
Lung Diseases, Interstitial*;
Pneumocytes;
Pulmonary Fibrosis;
Sarcoidosis;
Transforming Growth Factor beta;
Up-Regulation
- From:Tuberculosis and Respiratory Diseases
1996;43(2):164-172
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Transforming growth factor-beta(TGF-beta) may play a role in a variety of fibroproliferative disorders including pulmonary fibrosis via the induction of extracellular matrix accumulation. TGF-beta not only stimulates extracellular matrix production, but also decreases matrix degradation. Interstial lung diseases have demonstrated marked expression of TGF-beta. METHODS: To evaluate the possible role of TGF-beta in human pulmonary fibrosis, by using neutralizing antibody of TGF-beta we investigated immunohistochemically the expression of TGF-beta in the formalin-fixed, paraffin-embedded tissue sections of the 5 normal cases for the control, and a couple of pieces of tissues taken out of 3 cases with idiopathic pulmonary fibrosis, 3 cases with ILD from bleomycin toxicity, 3 cases with ILD from sarcoidosis, and 3 cases with ILD from eosinophilic granuloma. RESULTS: In the 5 normal cases for the control, the TGF-beta was expressed in bronchial and alveolar epithelial cells. Up-regulation of the TGF-3 expression was showed in the interstitial fibroblast cells of alveolar septa in 5 pieces and proliferated alveolar pneumocytes in 1 piece among 6 pieces tissues taken out of 3 cases with idiopathic pulmonary fibrosis. Also up-regulation of the TGF-beta expression was showed in alveolar lining pneumocytes, intra-alveolar mononuclear cells, and epithelioid cells in most of cases of ILD from bleomycin toxicity, sarcoidosis and eosinophilic granuloma. CONCLUSION: These findings suggest that up-regulation of the TGF-beta are involved in pathogenesis of interstitial lung fibrosis from variety of causes.
