Interaction of asbestos with alveolar cells

Our plain-English summary of Interaction of asbestos with alveolar cells, by Y. Suzuki (Environmental Health Perspectives, 1974).

The study

• Author: Y. Suzuki
• Journal: Environmental Health Perspectives
• Published: 1974;9:241-52
• Cited by: 23 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

A number of electron microphotographs are presented showing the various aspects of phagocytosis of fibers in lung tissue. The fibers were rapidly phagocytosed by alveolar macrophages, by polymorphonuclear leucocytes, and less frequently by alveolar epithelial cells. They were also found in the cytoplasm of the alveolar stromal macrophages. In the late stage of the disease, macrophages containing the minerals were recognized in the fibrous submesothelial connective tissues. In this stage, a cell intermediate in structure between the epithelial cell and the macrophage was observed in the alveolar lining. This cell showed strong phagocytic activity against the fibers. The process of phagocytosis of the fibers was quite similar to that of other microparticles such as Thorotrast and India ink. It had been suggested that phagosomes containing the fibers became transformed into secondary lysosomes. The fate of the phagocytosed fibers varied. Some were partly dissolved or digested with marked reduction in the thickness of the wall of the chrysotile fibril. Many became coated by hemosiderin which accumulated in the cytoplasm of the phagocytic cells. This coating transformed the fibers into asbestos bodies. Finally many fibers were released because of the death of the host cell. Uncoated fibers as well as various stages of phagocytosis were observed in all animals, including those 1 to 2 years after the instillation of asbestos. This strongly suggests that fibers may be repeatedly phagocytosed, released and rephagocytosed, inducing a continuous response of the alveolar cells and maintaining the disease.

In plain English

This was an animal experiment reporting electron microscope pictures of hamster lungs exposed to asbestos. Sixty male hamsters each received a single dose of 1-2 mg of chrysotile, amosite or crocidolite asbestos placed into the windpipe. The animals were killed either 1 to 28 days later or 6 months to 2 years later, and their lungs were examined under light and electron microscopes. Early on, clusters of macrophages and other white blood cells gathered in the air sacs and quickly engulfed the fibers. Cells lining the air sacs did so less often. Later, the lungs showed giant cells, asbestos bodies and fibrosis. Engulfed fibers met different fates. Some chrysotile fibrils appeared partly digested. Many became coated, apparently by hemosiderin, an iron-containing material, forming asbestos bodies, with immature ones seen as early as 16 days. Others were released when the host cell died. Uncoated fibers were still seen in all animals, including those examined 1 to 2 years after exposure. The author concluded this strongly suggests fibers are repeatedly engulfed, released and re-engulfed, keeping the disease going. The article gave no counts by fiber type or time point.

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: animal experiment (intratracheal instillation in hamsters, examined by light and electron microscopy)
• Who was studied: 60 male hamsters, killed in the early stage (1 to 28 days after instillation) or the late stage (6 months to 2 years); work done at Mt. Sinai Medical School, New York
• Exposure: a single intratracheal dose of 1-2 mg of chrysotile, amosite or crocidolite asbestos suspended in 0.1 ml of normal saline
• Main results:
  • Fibers were rapidly engulfed (phagocytosed) by alveolar macrophages and polymorphonuclear leucocytes, and less frequently by alveolar epithelial cells
  • The early acute inflammatory reaction was later replaced by proliferative changes, with multinucleated giant cells and, 6 months to one year afterwards, asbestos bodies and pulmonary fibrosis
  • A giant phagocytic cell in the alveolar lining kept structural features of an epithelial cell, which the author took as strongly suggesting that alveolar epithelium can transform into phagocytic cells
  • One phagocytosed chrysotile fibril was extremely reduced in thickness, suggesting partial digestion
  • Immature asbestos bodies were found as early as 16 days after instillation; the author suggested hemosiderin is the source of the coating
  • Some host cells died rapidly and released virtually unaltered fibers
  • Uncoated fibers and various stages of phagocytosis were seen in all animals, including those 1 to 2 years after instillation
• The authors' conclusion: The author concluded that the findings strongly suggest fibers may be repeatedly phagocytosed, released and rephagocytosed, inducing a continuous response of alveolar cells and maintaining the disease

Topics

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

Medical terms in this study, explained in our Lexicon: Phagocytosis, Alveolar Macrophage, Macrophage, Chrysotile, Fibril, Asbestos Bodies.

Related studies

• Phagocytic activity of the alveolar epithelial cells in pulmonary asbestosis — Y. Suzuki, J. Churg, et al. (1972)
• Pulmonary cell interactions with asbestos fibers in vivo and in vitro — A.R. Brody (1986)
• Asbestos effects on superoxide production. An in vitro study of hamster alveolar macrophages — B.W. Case, M.P. Ip, et al. (1986)
• In vitro biodegradation of chrysotile fibres by alveolar macrophages and mesothelial cells in culture: comparison with a pH effect — M.C. Jaurand, A. Gaudichet, et al. (1984)
• Mitochondria-targeted Ogg1 and aconitase-2 prevent oxidant-induced mitochondrial DNA damage in alveolar epithelial cells — S.J. Kim, P. Cheresh, et al. (2014)
• Changes in DNA 8-hydroxyguanine levels, 8-hydroxyguanine repair activity, and hOGG1 and hMTH1 mRNA expression in human lung alveolar epithelial cells induced by crocidolite asbestos — H.N. Kim, Y. Morimoto, et al. (2001)

Browse more research in Environmental Health Perspectives, or return to medical research.