| Silica induced Expression of IL-1beta, IL-6, TNF-beta, TGF-alpha, in the Experimental Murine Lung Fibrosis. |
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Shin Young Ki, Sung Woo Park, Myung Ran Lee, Eun Young Kim, Soo Taek Uh, Yong Hoon Kim, Choon Sik Park, Hi Bal Lee |
1Department of Internal Medicine, College of Medicine, Soonchunhyang University, Seoul, Korea.
2Hyonam Kidney Laboratory, Soonchunhyang University, Seoul, Korea. |
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| Abstract |
BACKGROUND
Silica-induced lung diseases is characterized by the accumulation of inflammatory cells at early stage and fibrosis in pulmonary parenchyma and interstitium at late stage. As a consequence of inflammation, silicosis is accompanied with the expansion of interstitial collagen and the formation of fibrotic nodule. In this process, several kinds of lung cells produce cytokines which can amplify and modulate pulmonary fibrosis. The alveolar macrophage is a potent source of proflammatory cytokines and growth factor. But in the process of silicotic inflammation and fibrosis, there are many changes of the kinetics in cytokine network. And the sources of cytokines in each phase are not well mown. METHOD: 2.5 mg of silica was instillated into the lung of C57BL/6J mice. After intratracheal instillation of silica, the lungs were removed for imunohistsochemical stain at 1. 2,7 day, 2, 4,8, 12 week, respecilvely. We investigated the expression of IL-1beta, IL-6, TNF-alpha and TGF-beta in lung tissue. RESULTS: 1) The expression of IL-6 increased from 1 day after exposure to S weeks in vascular endothelium. Also peribronchial area were stained for IL-6 from 7 days and reached the peak level for 4 weeks. 2) The IL-1beta was expressed weakly at the alveolar and peribronchial area through 12 weeks. 3) The TNF- expressed strongly at alveolar and bronchial epithelia during early stage and maintained for 12 weeks. 4) TGF-beta was expressed strongly at bronchial epithelia and peribronchial area after 1 week and the strongest at 8 weeks. CONCLUISON: The results above suggests IL-6, TNF- appear to be a early inflammatory response in silica induced lung fibrosis and TGF-beta play a major role in the maintenance and modulation of fibrosis in lung tissue. And the regulation of TNF- production will be a key role in modultion of silica-induced fibrosis. |
| Key Words:
silica, fibrosis, macrophage, immunohistochemical stain, TNF-alpha, TGF-beta |
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