Tuberculosis and Respiratory Diseases
- 제45권4호
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- Pages.835-845
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- 1998
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- 1738-3536(pISSN)
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- 2005-6184(eISSN)
유리규산에 의한 폐장내 IL-1$\beta$ , IL-6, TNF-$\alpha$ , TGF-$\beta$ 의 발현
Silica induced Expression of IL-1$\beta$ , IL-6, TNF-$\beta$ , TGF-$\alpha$ , in the Experimental Murine Lung Fibrosis
- 기신영 (순천향대학교 의과대학 내과학교실, 현암신장연구소) ;
- 박성우 (순천향대학교 의과대학 내과학교실, 현암신장연구소) ;
- 이명란 (순천향대학교 의과대학 내과학교실, 현암신장연구소) ;
- 김은영 (순천향대학교 의과대학 내과학교실, 현암신장연구소) ;
- 어수택 (순천향대학교 의과대학 내과학교실, 현암신장연구소) ;
- 김용훈 (순천향대학교 의과대학 내과학교실, 현암신장연구소) ;
- 박춘식 (순천향대학교 의과대학 내과학교실, 현암신장연구소) ;
- 이희발 (순천향대학교 의과대학 내과학교실, 현암신장연구소)
- Ki, Shin-Young (Department of Internal Medicine, College of Medicine, Hyonam Kidney Laboratory, Soonchunhyang University) ;
- Park, Sung-Woo (Department of Internal Medicine, College of Medicine, Hyonam Kidney Laboratory, Soonchunhyang University) ;
- Lee, Myung-Ran (Department of Internal Medicine, College of Medicine, Hyonam Kidney Laboratory, Soonchunhyang University) ;
- Kim, Eun-Young (Department of Internal Medicine, College of Medicine, Hyonam Kidney Laboratory, Soonchunhyang University) ;
- Uh, Soo-Taek (Department of Internal Medicine, College of Medicine, Hyonam Kidney Laboratory, Soonchunhyang University) ;
- Kim, Yong-Hoon (Department of Internal Medicine, College of Medicine, Hyonam Kidney Laboratory, Soonchunhyang University) ;
- Park, Choon-Sik (Department of Internal Medicine, College of Medicine, Hyonam Kidney Laboratory, Soonchunhyang University) ;
- Lee, Hi-Bal (Department of Internal Medicine, College of Medicine, Hyonam Kidney Laboratory, Soonchunhyang University)
- 발행 : 1998.08.30
초록
연구배경: 유리규산(silica)이 폐장내로 흡입되면 폐장내 염증세포의 축적이 발생하고 폐실질과 간질에 섬유화가 발생한다. Silica가 폐장내로 흡입되면 대삭세포에 탐식되어 염증매개물을 분비한다. 대식세포에서 염증반응에 중요하게 관여히는 cytokines은 IL-1
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 known. 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 imunohistochemical stain at 1, 2, 7 day, 2, 4, 8, 12 week, respectively. We investigated the expression of IL-1