Inflammation and asbestosis: characterization and maintenance of alveolitis following acute asbestos exposure

Our plain-English summary of Inflammation and asbestosis: characterization and maintenance of alveolitis following acute asbestos exposure, by C. Schoenberger, G. Hunninghake, J. Gadek, et al (Chest, 1981).

The study

• Authors: C. Schoenberger, G. Hunninghake, J. Gadek, R. Crystal
• Journal: Chest
• Published: 1981;80(1 Suppl):70-1
• Cited by: 14 articles, as counted by NIH iCite
• Read it: PubMed · Publisher
• In J-M's library: Johns-Manville's company medical library held a copy (J-M no. 001982).

Summary of the article

This short conference report from the National Heart, Lung and Blood Institute, Bethesda, asked whether asbestos fibers trigger an acute inflammatory response in the lung. Guinea pigs received a single intratracheal injection of 25 mg of chrysotile asbestos fibers in 1 ml of saline, or 1 ml of saline alone. The number of animals was not stated. At four hours and ten days after injection, the authors examined lung tissue by light microscopy and analysed cells recovered by bronchoalveolar lavage (BAL). Lungs of control animals had no neutrophils and small numbers of alveolar macrophages. Lungs of asbestos-treated animals showed peribronchial and alveolar collections of neutrophils and alveolar macrophages. BAL confirmed more neutrophils after asbestos than after saline: mean values were 28 versus 4 at four hours and 38 versus 10 at ten days. In a separate experiment, alveolar macrophages exposed to chrysotile in vitro for three hours released a chemotactic factor for neutrophils (53 ± 8 neutrophils/hpf), while unstimulated macrophages did not (5 ± 1 neutrophils/hpf). Coating the fibers beforehand with fresh normal serum increased this release. The authors concluded that asbestos causes an acute neutrophil-rich inflammatory response in the lung, that asbestos may attract neutrophils partly by stimulating alveolar macrophages to release a chemotactic factor, and that serum coating of the fibers may increase this release.

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 conference report from the National Heart, Lung and Blood Institute described an animal and laboratory experiment on how asbestos might inflame the lung. Guinea pigs received a single injection into the windpipe of 25 mg of chrysotile asbestos in saline, or saline alone. The number of animals was not given. Lungs and fluid washed from the lungs were examined at four hours and ten days. Compared with saline-treated animals, asbestos-treated animals had collections of neutrophils (a type of white blood cell) and alveolar macrophages in the lungs. Neutrophils also made up a larger share of lung-fluid cells (printed as 28 versus 4 at four hours, and 38 versus 10 at ten days); the plus-or-minus figures printed with these values are garbled in the scan. In the laboratory, fluid from macrophages exposed to chrysotile attracted 53 plus or minus 8 neutrophils per high-power field, versus 5 plus or minus 1 for unexposed macrophages. Coating the fibers with fresh serum increased release of this attracting factor. The authors concluded that asbestos results in an acute inflammatory lung response marked by neutrophils, and that macrophages may draw neutrophils in by releasing this factor.

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 (guinea pigs) combined with a laboratory (in vitro) study of alveolar macrophages; short conference report with recorded discussion
• Who was studied: Guinea pigs (number not stated), studied at the National Heart, Lung and Blood Institute, Bethesda; asbestos-injected animals compared with saline-injected control animals; alveolar macrophages studied in the laboratory
• Exposure: A single intratracheal injection of 25 mg of chrysotile asbestos fibers in 1 ml saline, versus 1 ml saline alone; in the laboratory, alveolar macrophages were exposed to chrysotile asbestos for three hours, with and without prior coating of the fibers with fresh normal serum
• Main results:
  • At both four hours and ten days, lungs of asbestos-treated animals showed peribronchial and alveolar collections of neutrophils and alveolar macrophages. Lungs of saline control animals had no neutrophils and small numbers of alveolar macrophages.
  • The proportion of lavage-fluid cells that were neutrophils was higher in asbestos-treated animals. Central values were printed as asbestos 28 versus saline 4 at four hours, and asbestos 38 versus saline 10 at ten days. The accompanying plus-or-minus figures and units are garbled by the scan, and the article does not say what the plus-or-minus terms represent.
  • Fluid (supernatant) from alveolar macrophages stimulated with asbestos showed neutrophil-attracting (chemotactic) activity of 53 plus or minus 8 neutrophils per high-power field. Fluid from unstimulated macrophages gave 5 plus or minus 1 neutrophils per high-power field, which the authors described as no chemotactic activity.
  • Coating the asbestos fibers beforehand with fresh normal serum increased release of the chemotactic factor from alveolar macrophages.
• The authors' conclusion: The authors concluded that asbestos results in an acute inflammatory lung response characterized by neutrophils. They concluded that one mechanism may be that asbestos stimulates alveolar macrophages to release a chemotactic factor for neutrophils, and that coating fibers with serum factors may augment this release.

Topics

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

Medical terms in this study, explained in our Lexicon: Inflammation, Asbestos Exposure, Chrysotile, Bronchoalveolar Lavage (BAL), Alveolar Macrophage, Macrophage.

Related studies

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• Extracellular superoxide dismutase inhibits inflammation by preventing oxidative fragmentation of hyaluronan — F. Gao, J.R. Koenitzer, et al. (2008)
• Role of alveolar macrophages in asbestosis: modulation of neutrophil migration to the lung after acute asbestos exposure — C.I. Schoenberger, G.W. Hunninghake, et al. (1982)
• Lung inflammation caused by inhaled toxicants: a review — J. Wong, B.E. Magun, et al. (2016)
• Inhalation and Oropharyngeal Aspiration Exposure to Rod-Like Carbon Nanotubes Induce Similar Airway Inflammation and Biological Responses in Mouse Lungs — P. Kinaret, M. Ilves, et al. (2017)
• Patterns of inflammation, cell proliferation, and related gene expression in lung after inhalation of chrysotile asbestos — T.R. Quinlan, K.A. BéruBé, et al. (1995)

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