Actin-containing microfilaments of pulmonary epithelial cells provide a mechanism for translocating asbestos to the interstitium

Our plain-English summary of Actin-containing microfilaments of pulmonary epithelial cells provide a mechanism for translocating asbestos to the interstitium, by A.R. Brody, L.H. Hill, W.S. Stirewalt, et al (Chest, 1983).

The study

• Authors: A.R. Brody, L.H. Hill, W.S. Stirewalt, K.B. Adler
• Journal: Chest
• Published: 1983;83(5 Suppl):11S-12S
• Cited by: 15 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Summary of the article

The authors proposed that actin-containing microfilaments in alveolar epithelial cells provide a mechanism for moving inhaled asbestos fibers into the lung interstitium, the compartment chiefly affected in asbestosis. White rats were exposed to a chrysotile asbestos aerosol for 1 hour and were killed immediately afterward and at 24 hours, 48 hours and 1 month. Lungs were perfusion-fixed for electron microscopy. Some fresh tissue was treated with glycerol and heavy meromyosin to stabilize microfilaments. In vitro, asbestos fibers were added to tracheal organ cultures and to an established tracheal epithelial cell line. These were examined by electron microscopy, and polymerized and non-polymerized actin were measured by a DNase I inhibition assay. Inhaled fibers were found inside type I alveolar epithelial cells from immediately after exposure through 48 hours. They were generally not membrane-bound and were associated with filaments about 50-70 Å in diameter. Heavy meromyosin-treated tissue showed web-like microfilament complexes around fibers, and cultured cells also showed filaments associated with fibers. In hamster tracheal epithelial cells, filamentous actin was 12% in untreated cells compared with 25% and 21% in cells treated with two amounts of chrysotile. The experiment was repeated twice with nearly identical results. The authors concluded that contractile microfilaments may supply the force that moves asbestos fibers through the epithelium to the interstitium, where they interact with fibroblasts and macrophages.

PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

In plain English

This was a short laboratory report combining a rat experiment with cell and tissue culture work. The authors tested their proposal that actin-containing microfilaments, fine protein strands inside the cells lining the lung's air sacs, move inhaled asbestos into the lung interstitium, the tissue behind that lining. White rats breathed an aerosol of chrysotile asbestos for 1 hour, and the authors examined the lungs by electron microscopy. Chrysotile fibers were seen inside type I alveolar epithelial cells from immediately after exposure through 48 hours. The fibers generally were not membrane-bound and were associated with filaments about 50-70 A in diameter. In tissue treated to stabilize these filaments, web-like filament complexes surrounded the fibers. Cultured tracheal epithelial cells and tracheal explants also showed filaments associated with asbestos fibers. In hamster tracheal epithelial cells, filamentous actin was 12% in untreated cells, 25% at the lower chrysotile dose and 21% at the higher dose. The experiment was repeated twice with nearly identical results. The authors proposed that contractile microfilaments provide the force that moves asbestos fibers through the epithelium to the interstitium.

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 study: an animal inhalation experiment in rats examined by electron microscopy, plus in vitro experiments on tracheal organ cultures and a tracheal epithelial cell line, including biochemical measurement of actin
• Who was studied: White rats (number not stated), killed immediately after exposure and at 24 hours, 48 hours and 1 month afterward; organ cultures of tracheal explants; cultured cells from an established tracheal epithelial cell line (hamster, according to Table 1)
• Exposure: Rats breathed an aerosol of chrysotile asbestos for only 1 hour; the scanned text garbles the concentration and its unit. In vitro, asbestos fibers were added to the cultures; Table 1 lists two chrysotile doses, with the unit garbled.
• Main results:
  • In rats, inhaled asbestos fibers were found inside the cytoplasm of type I alveolar epithelial cells immediately after the 1-hour exposure and through the 48-hour post-exposure period
  • In rat lung cells, the fibers generally were not enclosed in a membrane and were associated with intracellular filaments about 50-70 A in diameter
  • In rat lung tissue treated with heavy meromyosin, the authors commonly found web-like complexes of microfilaments around asbestos fibers inside the epithelial cells
  • Electron microscopy of cultured tracheal explants and epithelial cells showed filaments associated with asbestos fibers
  • In hamster tracheal epithelial cells, filamentous actin was 12% in untreated cells, 25% at the lower chrysotile dose and 21% at the higher dose (Table 1). The authors described this as substantially increased over the untreated controls and reported that the experiment was repeated twice with nearly identical results.
• The authors' conclusion: The authors proposed, as a hypothesis, that contractile actin-containing microfilaments provide the motive force that moves asbestos fibers through the epithelium to the lung interstitium. There the fibers interact with fibroblasts and macrophages, cell types the authors considered likely to play a major role in the development of asbestosis.
• Limitations the authors state:
  • Glycerol-treated lung tissue was generally swollen and disrupted, so only well-stabilized microfilament complexes survived preparation for electron microscopy

Topics

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

Medical terms in this study, explained in our Lexicon: Chrysotile, Epithelium, Fibroblast, Macrophage.

Related studies

• Distribution of transforming growth factor-beta 1, fibronectin, and smooth muscle actin in asbestos-induced pulmonary fibrosis in rats — T.D. Perdue, A.R. Brody (1994)
• Slug enhances invasion ability of pancreatic cancer cells through upregulation of matrix metalloproteinase-9 and actin cytoskeleton remodeling — K. Zhang, D. Chen, et al. (2011)
• Alteration of cytoskeletal molecules in a human T cell line caused by continuous exposure to chrysotile asbestos — M. Maeda, Y. Chen, et al. (2013)
• Actin polymerization plays a significant role in asbestos-induced inflammasome activation in mesothelial cells in vitro — M. MacPherson, C. Westbom, et al. (2017)
• Comparative immunohistochemical staining for desmin and muscle-specific actin. A study of 576 cases — S. Rangdaeng, L.D. Truong (1991)
• On the mechanism of cell internalization of chrysotile fibers: an immunocytochemical and ultrastructural study — W. Malorni, F. Iosi, et al. (1990)

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