Phagocytic activity of the alveolar epithelial cells in pulmonary asbestosis

Our plain-English summary of Phagocytic activity of the alveolar epithelial cells in pulmonary asbestosis, by Y. Suzuki, J. Churg, T. Ono (The American Journal of Pathology, 1972).

The study

• Authors: Y. Suzuki, J. Churg, T. Ono
• Journal: The American Journal of Pathology
• Published: 1972;69(3):373-88
• Cited by: 37 articles, as counted by NIH iCite
• Read it: PubMed · Free full text

Abstract

In the course of pulmonary asbestosis in hamsters, alveolar epithelial cells can transform into large phagocytic cells which ingest asbestos fibers and produce asbestos bodies. In the process, the epithelial cells frequently lose their original Type I or Type II cell structure and change into a form intermediate between the epithelial cell and the alveolar macrophage. This transformation may be the result of continuous stimulation of the cells by repeated phagocytosis of asbestos, followed by rapid death of the host cell, release of the fibers and rephagocytosis by a new cell. It is suggested that some of the large macrophages in the alveolar spaces originate from the alveolar epithelial cells via the intermediate form.

In plain English

This was an animal experiment. The authors placed 1 mg of chrysotile asbestos in saline directly into the windpipe of 24 male Syrian hamsters. They examined the lungs under light and electron microscopes at times from 1 day to 24 months afterward, and three more hamsters served as controls. Most fibers were taken up by scavenger cells (macrophages) and white blood cells, but some fibers were found inside the cells lining the air sacs (alveolar epithelial cells). These lining cells were often structurally changed, sometimes partly detached, and some became giant cells with several nuclei. Fibers inside them often looked partly dissolved, and asbestos bodies (coated fibers) formed in them much as in macrophages. The share of lining cells containing asbestos increased as the experiment went on, and uncoated fibers were still present 2 years after instillation. The article gave no cell counts. The authors proposed that in asbestosis some lung macrophages arise from lining cells through an intermediate form. They said it was uncertain whether this happens only under unusual circumstances.

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 (light and electron microscopy of hamster lungs after asbestos instillation)
• Who was studied: 24 male Syrian hamsters, killed at intervals from 1 day to 24 months after instillation, plus 3 control hamsters; Mount Sinai School of Medicine, New York
• Exposure: a single intratracheal instillation of 1 mg of chrysotile asbestos suspended in 0.1 ml of normal saline
• Main results:
  • Most fibers were taken up by alveolar and interstitial macrophages and polymorphonuclear leukocytes, but some fibers were found inside alveolar epithelial cells
  • Epithelial cells that had taken up fibers were often structurally altered and sometimes detached from the basement membrane
  • Fibers inside epithelial cells frequently showed partial dissolution or digestion, as seen in macrophages
  • The proportion of epithelial cells containing asbestos increased with the duration of the experiment (no counts given)
  • Asbestos bodies were found in the cytoplasm of epithelial cells, and some epithelial cells became multinucleated giant cells
  • Uncoated asbestos fibers were present in all three types of phagocytic cells as late as 2 years after instillation
  • No transitions were found between interstitial macrophages and the phagocytic epithelial cells
• The authors' conclusion: The authors concluded that under suitable conditions the alveolar epithelium can ingest particles. They proposed that in asbestosis at least some alveolar macrophages form by transformation of alveolar epithelial cells through an intermediate form.
• Limitations the authors state:
  • The authors said it was uncertain whether this transformation occurs only under unusual circumstances or is a common event
  • Once the intermediate cells detach into the air space, they can no longer be told apart from free alveolar macrophages
  • The material gave no direct clue to the origin of the interstitial macrophages

Topics

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

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

Related studies

• 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)
• Interaction of asbestos with alveolar cells — Y. Suzuki (1974)
• Production of reactive oxygen species by phagocytic cells after exposure to glass wool and stone wool fibres - effect of fibre preincubation in aqueous solution — T. Zoller, W.J. Zeller (2000)
• Mitochondria-targeted Ogg1 and aconitase-2 prevent oxidant-induced mitochondrial DNA damage in alveolar epithelial cells — S.J. Kim, P. Cheresh, et al. (2014)
• Mitochondrial catalase overexpressed transgenic mice are protected against lung fibrosis in part via preventing alveolar epithelial cell mitochondrial DNA damage — S.J. Kim, P. Cheresh, et al. (2016)
• Asbestos causes apoptosis in alveolar epithelial cells: role of iron-induced free radicals — A. Aljandali, H. Pollack, et al. (2001)

Browse more research in The American Journal of Pathology, or return to medical research.