Expression of Transforming Growth Factor-Beta in Patients with Interstitial Lung Diseases (ILD)
Sung Soo Park, Kyung Sang Lee, Suck Chul Yang, Ho Joo Yoon, Dong Ho Shin, Dong Hoo Lee, Jung Dal Lee, Jung Hee Lee
Abstract
Sung Soo Park, Kyung Sang Lee, Suck Chul Yang, Ho Joo Yoon, Dong Ho Shin, Dong Hoo Lee, Jung Dal Lee, Jung Hee Lee
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.
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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.
Key concepts: Pulmonary fibrosis, Bleomycin, Pathology, Medicine, Lung, Fibrosis, Extracellular matrix, Interstitial lung disease