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Involvement of Iron Homeostasis in Fibrotic Process of Smokers Lung
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A5768 - Involvement of Iron Homeostasis in Fibrotic Process of Smokers Lung
Author Block: S. Kunugi1, N. Kokuho1, N. Kokuho2, Y. Kajimoto1, M. Terasaki1, Y. Terasaki1; 1Department of Analytic Human Pathology, Nippon Medical School, Graduate School of Medicine, Tokyo, Japan, 2Department of Pulmonary Medicine and oncology, Nippon Medical School, Graduate School of Medicine, Tokyo, Japan.
RATIONALE: Iron is an essential element required for diverse biological processes such as respiration, DNA synthesis and energy production, and metabolism. It can also generate reactive oxygen species(ROS) that can damage biological macromolecules. To limit oxidative stress, iron acquisition and its distribution must be tightly regulated. In the lungs, excess iron accumulation has been reported in association with cigarette smoke, severe emphysema, acute respiratory distress syndrome, pulmonary alveolar proteinosis, and patient with lung transplant. In smokers, the histological hallmark is bronchiolocentric cluster of pigmented macrophage. Air space enlargement with fibrosis is a relatively recent described pathological pattern. This term was initially used to describe changes observed in non-neoplastic lung parenchyma in lobectomy specimen from smokers with cancer. The mechanism involved in pulmonary iron deposition and its role in the vivo pathogenesis of lung fibrotic process in smokers remains unknown. METHODS: We analyzed the expression profiles of iron related proteins (Ferritin, Ferroportin, Iron-regulatory protein 2; IRP2. and F-box/LRR-repeat protein 5; FBXL5) in the lung tissues from non-neoplastic lung parenchyma in lobectomy specimen from smokers and non-smokers with cancer. Non heme iron expression was detected by berlin blue staining with subsequent quantitative assessment was achieved by a light microscopy and computer-based semi-automatic software. Immunohistochemistry for Oxidative stress maker (8-OhdG) were performed. Result: Compared with non-smokers lungs, iron deposition and immunoreactivity for iron related proteins were increased in pigmented alveolar macrophages in smokers lungs, although immunoreactivity for 8-OhdG were not. Iron deposition in bronchiolar and alveolar epithelial cells were not observed, but immunoreactivity for iron-related proteins and 8-OhdG were increased. CONCLUSIONS: Iron sequestration in alveolar macrophages in fibrotic process of smokers lungs will be discussed.
Author Block: S. Kunugi1, N. Kokuho1, N. Kokuho2, Y. Kajimoto1, M. Terasaki1, Y. Terasaki1; 1Department of Analytic Human Pathology, Nippon Medical School, Graduate School of Medicine, Tokyo, Japan, 2Department of Pulmonary Medicine and oncology, Nippon Medical School, Graduate School of Medicine, Tokyo, Japan.
RATIONALE: Iron is an essential element required for diverse biological processes such as respiration, DNA synthesis and energy production, and metabolism. It can also generate reactive oxygen species(ROS) that can damage biological macromolecules. To limit oxidative stress, iron acquisition and its distribution must be tightly regulated. In the lungs, excess iron accumulation has been reported in association with cigarette smoke, severe emphysema, acute respiratory distress syndrome, pulmonary alveolar proteinosis, and patient with lung transplant. In smokers, the histological hallmark is bronchiolocentric cluster of pigmented macrophage. Air space enlargement with fibrosis is a relatively recent described pathological pattern. This term was initially used to describe changes observed in non-neoplastic lung parenchyma in lobectomy specimen from smokers with cancer. The mechanism involved in pulmonary iron deposition and its role in the vivo pathogenesis of lung fibrotic process in smokers remains unknown. METHODS: We analyzed the expression profiles of iron related proteins (Ferritin, Ferroportin, Iron-regulatory protein 2; IRP2. and F-box/LRR-repeat protein 5; FBXL5) in the lung tissues from non-neoplastic lung parenchyma in lobectomy specimen from smokers and non-smokers with cancer. Non heme iron expression was detected by berlin blue staining with subsequent quantitative assessment was achieved by a light microscopy and computer-based semi-automatic software. Immunohistochemistry for Oxidative stress maker (8-OhdG) were performed. Result: Compared with non-smokers lungs, iron deposition and immunoreactivity for iron related proteins were increased in pigmented alveolar macrophages in smokers lungs, although immunoreactivity for 8-OhdG were not. Iron deposition in bronchiolar and alveolar epithelial cells were not observed, but immunoreactivity for iron-related proteins and 8-OhdG were increased. CONCLUSIONS: Iron sequestration in alveolar macrophages in fibrotic process of smokers lungs will be discussed.
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