2002PubMedRequires access

[The role of transforming growth factor-beta(1) in smoking-induced chronic bronchitis and emphysema in hamsters].

Li Li, Ying-mao Ruan, Ying Chen, Yan Chu, Xinlin Xu

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Abstract

OBJECTIVE: To study the role of transforming growth factor-beta(1) (TGF-beta(1)) in the pathogenesis of chronic bronchitis and emphysema. METHODS: An animal model of chronic bronchitis and emphysema was developed in hamsters by chronic smoke inhalation. The expression of TGF-beta(1) mRNA and protein in the pulmonary tissue was observed. The bronchial epithelia was stimulated with cigarette smoke extract (CSE) in vitro and the expression of TGF-beta(1) was measured. RESULTS: 3 months after smoking, the animals developed chronic bronchitis and emphysema. TGF-beta(1) immunoreactivity in the pulmonary tissue and cultured bronchial epithelia increased significantly as compared to the normal control (2.75 +/- 0.23 vs 0.84 +/- 0.39, P = 0.001 and 2.67 +/- 0.16 vs 0.85 +/- 0.54, P = 0.001). The expression of TGF-beta(1) mRNA was also increased in the animal model (1.28 vs 0.98). CONCLUSIONS: Smoking can induce over-expression of TGF-beta(1) in bronchial epithelia, which may be one of the mechanisms for smoking-induced chronic bronchitis and emphysema.

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OBJECTIVE: To study the role of transforming growth factor-beta(1) (TGF-beta(1)) in the pathogenesis of chronic bronchitis and emphysema. METHODS: An animal model of chronic bronchitis and emphysema was developed in hamsters by chronic smoke inhalation. The expression of TGF-beta(1) mRNA and protein in the pulmonary tissue was observed. The bronchial epithelia was stimulated with cigarette smoke extract (CSE) in vitro and the expression of TGF-beta(1) was measured. RESULTS: 3 months after smoking, the animals developed chronic bronchitis and emphysema. TGF-beta(1) immunoreactivity in the pulmonary tissue and cultured bronchial epithelia increased significantly as compared to the normal control (2.75 +/- 0.23 vs 0.84 +/- 0.39, P = 0.001 and 2.67 +/- 0.16 vs 0.85 +/- 0.54, P = 0.001). The expression of TGF-beta(1) mRNA was also increased in the animal model (1.28 vs 0.98). CONCLUSIONS: Smoking can induce over-expression of TGF-beta(1) in bronchial epithelia, which may be one of the mechanisms for smoking-induced chronic bronchitis and emphysema.

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Available abstract

OBJECTIVE: To study the role of transforming growth factor-beta(1) (TGF-beta(1)) in the pathogenesis of chronic bronchitis and emphysema. METHODS: An animal model of chronic bronchitis and emphysema was developed in hamsters by chronic smoke inhalation. The expression of TGF-beta(1) mRNA and protein in the pulmonary tissue was observed. The bronchial epithelia was stimulated with cigarette smoke extract (CSE) in vitro and the expression of TGF-beta(1) was measured. RESULTS: 3 months after smoking, the animals developed chronic bronchitis and emphysema. TGF-beta(1) immunoreactivity in the pulmonary tissue and cultured bronchial epithelia increased significantly as compared to the normal control (2.75 +/- 0.23 vs 0.84 +/- 0.39, P = 0.001 and 2.67 +/- 0.16 vs 0.85 +/- 0.54, P = 0.001). The expression of TGF-beta(1) mRNA was also increased in the animal model (1.28 vs 0.98). CONCLUSIONS: Smoking can induce over-expression of TGF-beta(1) in bronchial epithelia, which may be one of the mechanisms for smoking-induced chronic bronchitis and emphysema.

Key concepts: Chronic bronchitis, Medicine, Bronchitis, Pathogenesis, Transforming growth factor beta, BETA (programming language), Pulmonary emphysema, Internal medicine

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