2006 Fiscal Year Final Research Report Summary
Pathological Study of Interstitial Lung Diseases by Electron Probe Microanalyzer Equipped with a Wavelength Dispersive Spectrometer and Immunohistochemistry
| Project/Area Number |
16590740
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Niigata University |
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Principal Investigator |
SUZUKI Eiichi Niigata University, Medical and Dental Hospital, Professor, 医歯学総合病院, 教授 (30187710)
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| Co-Investigator(Kenkyū-buntansha) |
TAKADA Toshinori Niigata University, Institute of Medicine and Dentistry, Lecturer, 医歯学系, 講師 (40361919)
WATANABE Koichi Niigata University, Institute of Medicine and Dentistry, Associate Prof., 医歯学系, 助教授 (20018766)
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| Project Period (FY) |
2004 – 2006
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| Keywords | electron probe microanalyzer / hard metal lung disease / interstitial lung disease / immunohistochemistry |
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| Research Abstract |
Hard metal lung disease (HMLD) is caused by exposure to hard metal, a synthetic compound that combines tungsten carbide with cobalt as well as a number of other metals. Interstitial lung disease caused by hard metal is uniquely characterized by giant cell interstitial pneumonia. The pathogenesis of HMLD is unclear. To elucidate the distribution of inhaled hard metal and reactive inflammatory cells, we studied biopsy lung tissue from patients with HMLD using an electron probe microanalyzer equipped (EPMA) with a wavelength dispersive spectrometer (WDS) and immunohistochemistry. Seventeen patients with interstitial lung disease in which tungsten was detected and five controls were enrolled. Detection and mapping of elements were performed by an EPMA with WDS. We immunohistochemically stained mononuclear cells in tissues from five available cases with anti-human CD4, CD8, CD20, CD68, and CD 163 antibodies, and compared the distribution of positive cells with hard metal elements. Thirteen
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out of 17 patients were pathologically diagnosed as having giant cell interstitial pneumonia. Tungsten and cobalt were accumulated in the centrilobular fibrotic lesions, but never found in the control lungs. CD8^+ lymphocytes and CD163^+ monocyte-macrophages were predominantly distributed in centrilobular fibrotic lesions around the hard metal elements, and some of them were likely to colocalize with tungsten element. Small numbers of CD8+ and CD 163^+ cells were also immunohistochemically shown in peribronchiolar areas and alveolar walls. These results suggest that macrophages may phagocytose inhaled tungsten via CD 163 and play an important role in forming the fibrotic lesion of HMLD with cytotoxic T lymphocytes. In addition to the qualitative mapping of elements in lung tissue, we are detecting elements in a semiquantitative manner with an image analysis software. We are also analyzing element in lung tissue from patients with idiopathic pulmonary fibrosis (IPF) to study the relationship between inhaled elements and development of IPF. Less
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Research Products
(2 results)
