Analysis on the co-localization of asbestos bodies and Fas or CD163 expression in asbestos lung tissue by in-air micro-pixe

Our plain-English summary of Analysis on the co-localization of asbestos bodies and Fas or CD163 expression in asbestos lung tissue by in-air micro-pixe, by S. Matsuzaki, Y. Shimizu, K. Dobashi, et al (International Journal of Immunopathology and Pharmacology, 2010).

The study

• Authors: S. Matsuzaki, Y. Shimizu, K. Dobashi, T. Nagamine, T. Satoh, T. Ohkubo, A. Yokoyama, Y. Ishii, T. Kamiya, K. Arakawa, S. Makino, M. Utsugi, T. Ishizuka, S. Tanaka, K. Shimizu, M. Mori
• Journal: International Journal of Immunopathology and Pharmacology
• Published: 2010;23(1):1-11
• Cited by: 9 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

To prevent and control disease caused by exposure to various agents, it is necessary to determine the harmful level of intervention and to establish a method for measuring that level. In-air microparticle-induced X-ray emission (in-air micro-PIXE) analysis is based on irradiation of specimens with a proton ion microbeam, and has been modified for biological application. Two-dimensional analysis and quantitative analysis using the system confirmed that asbestos induced apoptosis by upregulating Fas expression and also revealed the accumulation of CD163-expressing macrophages in the lungs of patients with asbestosis. By quantitative comparison of the area of Fas or CD163 expression and the Fas- or CD163-negative area in asbestos lung tissue, the harmful levels which caused the expression of Fas or CD163 could be estimated on Silica, Ferrous iron, and Magnesium (the components of asbestos) deposition. These results indicate that the system could be useful for investigating the pathogenesis of inhaled particle-induced immune reactions and for determining harmful levels of exogenous agents.

In plain English

This laboratory study from Gunma University, Japan, examined lung tissue from four men who had surgery for lung adenocarcinoma. Two had asbestosis from occupational exposure, and two were controls without asbestos exposure. The authors analyzed non-tumorous lung tissue with in-air micro-PIXE, a proton-beam technique that maps elements such as silicon, iron and magnesium. They compared these maps with tissue staining for two proteins, Fas and CD163. In the asbestosis lungs, asbestos bodies sat at the same sites as lymphocytes expressing Fas and macrophages expressing CD163. From element ratios, the authors judged the fibers probably crocidolite at one site and probably amosite at the other. Control lungs showed no asbestos bodies, no Fas expression and only weak CD163 expression. In Fas-expressing areas, the ratio of silicon to background sulfur was 3.65±0.25 in asbestosis tissue versus 1.25±0.17 in control tissue. Within asbestosis tissue, it was higher in damaged than in intact areas. The authors concluded there is a harmful level above which asbestos causes tissue damage. They said the small sample makes their levels difficult to apply more widely.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Laboratory tissue study (elemental analysis by in-air micro-PIXE combined with H-E staining and immunohistochemistry) comparing surgical lung specimens from asbestosis patients and controls
• Who was studied: 4 men with lung adenocarcinoma who had surgical resection, studied at Gunma University, Japan: 2 with asbestosis (aged 68±2.8 years) and 2 controls without asbestos exposure (aged 71±2.8 years); non-tumorous lung tissue was analyzed. Study dates not given.
• Exposure: Occupational asbestos exposure (jobs not described). Fiber type was estimated from silicon, iron and magnesium ratios: probably crocidolite at the Fas-expressing site and probably amosite at the CD163-expressing site.
• Main results:
  • Silicon, iron and magnesium peaks were higher in asbestosis lung tissue than in control lung tissue.
  • In asbestosis lung, asbestos bodies were located at sites where lymphocytes expressing Fas had accumulated. The asbestos there was judged probably crocidolite.
  • In asbestosis lung, asbestos bodies were located at sites where macrophages expressing CD163 had accumulated. The asbestos there was judged probably amosite.
  • Control lungs showed no Fas expression, only weak CD163 expression by macrophages, and no asbestos bodies.
  • Silicon-to-sulfur ratio, asbestosis lung versus control lung: 3.65±0.25 versus 1.25±0.17 in Fas-expressing areas, and 4.59±0.90 versus 1.08±0.12 in CD163-expressing areas.
  • Within asbestosis lung, Fas-expressing damaged areas versus intact areas without Fas expression had a silicon-to-sulfur ratio of 3.65±0.25 versus 1.51±0.17.
  • Within asbestosis lung, CD163-expressing damaged areas versus intact areas had silicon-to-sulfur ratios of 4.59±0.90 versus 2.39±0.42, and iron-to-sulfur ratios of 0.23±0.11 versus 0.03±0.01.
  • Iron-to-sulfur and magnesium-to-sulfur ratios were significantly higher in CD163-expressing areas than in Fas-expressing areas.
• The authors' conclusion: The authors concluded that there is a harmful level of asbestos deposition above which tissue damage occurs, and that the in-air micro-PIXE system is possibly useful for determining such levels.
• Limitations the authors state:
  • The sample was small, so the harmful levels found are difficult to apply more widely. A larger group is needed.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Asbestosis.

Medical terms in this study, explained in our Lexicon: Asbestos Bodies, Apoptosis, Macrophage, Deposition.

Related studies

• In-air micro-particle induced X-ray emission analysis of asbestos and metals in lung tissue — Y. Shimizu, K. Dobashi, et al. (2008)
• Environmental scanning electron microscopy technique to identify asbestos phases inside ferruginous bodies — A. Croce, M. Musa, et al. (2013)
• Expression and activity of urokinase and its receptor in endothelial and pulmonary epithelial cells exposed to asbestos — A. Barchowsky, R.R. Roussel, et al. (1998)
• Elemental and immunohistochemical analysis of the lungs and hilar lymph node in a patient with asbestos exposure, a pilot study — Y. Koga, T. Satoh, et al. (2016)
• Study of inorganic particles, fibers, and asbestos bodies by variable pressure scanning electron microscopy with annexed energy dispersive spectroscopy and micro-Raman spectroscopy in thin sections of lung and pleural plaque — C. Rinaudo, A. Croce, et al. (2010)
• Asbestos upregulates expression of the urokinase-type plasminogen activator receptor on mesothelial cells — R.C. Perkins, V.C. Broaddus, et al. (1999)

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