Role of alveolar macrophages in asbestosis: modulation of neutrophil migration to the lung after acute asbestos exposure

Our plain-English summary of Role of alveolar macrophages in asbestosis: modulation of neutrophil migration to the lung after acute asbestos exposure, by C.I. Schoenberger, G.W. Hunninghake, O. Kawanami, et al (Thorax, 1982).

The study

• Authors: C.I. Schoenberger, G.W. Hunninghake, O. Kawanami, V.J. Ferrans, R.G. Crystal
• Journal: Thorax
• Published: 1982;37(11):803-9
• Cited by: 64 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

After intratracheal injection of short chrysotile asbestos fibres in guinea-pigs an intense neutrophil alveolitis was observed within three days. Evaluation by bronchoalveolar lavage of the inflammatory and immune effector cells producing the alveolitis by three days showed an increased proportion of polymorphonuclear leucocytes, which comprised 21% +/- 3% of the total leucocytes compared with 9% +/- 2% for the controls (p less than 0.05), persisting for at least six weeks (after which time the polymorphonuclear leucocytes comprised 28% +/- 2% compared with 7% +/- 1% for the controls: p less than 0.05). One mechanism by which asbestos fibres may cause polymorphonuclear leucocytes to be attracted to the alveolar structures is by induced release of neutrophil chemotactic factor by alveolar macrophages. When exposed in vitro to short or intermediate chrysotile fibres or amosite or crocidolite fibres guinea-pig alveolar macrophages released appreciable amounts of neutrophil chemotactic factor. The release of this chemotactic factor was augmented when the asbestos fibres had been previously exposed to normal serum. The chemotactic factor was lipid soluble, and was similar to the neutrophil chemotactic factor spontaneously released by alveolar macrophages recovered from guinea-pigs exposed in vivo to short chrysotile fibres. These observations suggest that alveolar macrophages may play an important part in the early stages of asbestosis by modulating the migration of neutrophils to the lung.

In plain English

In this guinea-pig and laboratory study, the authors injected 25 mg of short chrysotile asbestos into the windpipes of 30 guinea-pigs. They compared them with 40 controls given saline or no injection and examined the lungs three days, two weeks and six weeks later. The asbestos-injected animals developed inflammation of the air sacs involving neutrophils and eosinophils (types of white blood cell). In lung washings, these white cells made up an average of 21% of cells at three days compared with 9% in controls, and 28% compared with 7% at six weeks (p less than 0.05). In laboratory dishes, lung scavenger cells (alveolar macrophages) from normal guinea-pigs released a factor that attracts neutrophils when exposed to short or intermediate chrysotile, amosite or crocidolite. More was released when the fibres had first been coated with normal human serum. Macrophages from guinea-pigs injected with short chrysotile three days earlier released the factor without further exposure. The authors concluded that some lung changes of asbestosis may arise from asbestos stimulating macrophages to attract neutrophils, provided the guinea-pig model reflects inhaled asbestos in humans.

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 injection in guinea-pigs) combined with in vitro (laboratory dish) experiments on guinea-pig alveolar macrophages
• Who was studied: NIH strain guinea-pigs weighing 200-300 g: 30 exposed to asbestos and 40 controls (intratracheal saline or no injection), killed at three days, two weeks and six weeks. Alveolar macrophages from normal guinea-pigs were used for the laboratory experiments.
• Exposure: In the animals: 25 mg of short chrysotile (90% of fibres under 5 micrometres long) in 1 ml saline, injected intratracheally. In the laboratory: macrophages exposed to short-range chrysotile, intermediate-range chrysotile, amosite or crocidolite at two concentrations, with and without prior coating of the fibres in normal human serum.
• Main results:
  • At three days after injection, polymorphonuclear leucocytes made up 21% plus or minus 3% of lung-washing cells in asbestos-injected animals, compared with 9% plus or minus 2% in controls (p less than 0.05).
  • At six weeks, polymorphonuclear leucocytes made up 28% plus or minus 2% of lung-washing cells in asbestos-injected animals, compared with 7% plus or minus 1% in controls (p less than 0.05).
  • Under the microscope, lungs of asbestos-injected animals showed a widespread acute alveolitis at three days, with neutrophils and eosinophils in the air spaces. Inflammation was still present, more focal, at 14 and 42 days, and thickening of the alveolar walls was more pronounced at 42 days. Saline-injected animals had normal lungs.
  • Lymphocytes were 2% or less of lung-washing cells in both asbestos-injected and saline-injected animals at all time points (no significant difference).
  • In the laboratory, normal guinea-pig alveolar macrophages released significantly more neutrophil chemotactic factor with each of the four fibre types (short chrysotile, intermediate chrysotile, amosite, crocidolite) than with medium alone. Differences between the two fibre concentrations were not statistically significant.
  • Pre-coating the fibres with normal human serum increased release of the chemotactic factor for every fibre type at both concentrations (p less than 0.05).
  • With short chrysotile, macrophage supernatants attracted 94.4 plus or minus 4.8 neutrophils per high-power field, compared with 5.7 plus or minus 2.0 for macrophages incubated alone. The ethyl acetate (lipid) extract attracted 62.8 plus or minus 5.0, indicating the factor was at least partly lipid soluble.
  • Alveolar macrophages taken from guinea-pigs injected with short chrysotile three days earlier spontaneously released the neutrophil chemotactic factor. Macrophages from saline-injected controls did not (p less than 0.05; three animals per group shown in Fig 4).
• The authors' conclusion: The authors concluded that their observations suggest at least some of the damage to the alveolar structures associated with asbestosis is mediated by asbestos fibres stimulating alveolar macrophages to attract neutrophils to the lower respiratory tract.
• Limitations the authors state:
  • The findings apply to humans only to the extent that intratracheal injection in guinea-pigs is a valid model of inhaled asbestosis in humans.
  • In some animals the inflammation was confined to discrete areas of the lungs, which the authors suggested was perhaps a result of the method of asbestos exposure.
  • It was not clear which serum components were responsible for the increased release of the chemotactic factor.
  • The role of neutrophils in the development of asbestosis has not been evaluated in detail.

Topics

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

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

Related studies

• Effects of asbestos on the random migration of rabbit alveolar macrophages — Q.N. Myrvik, E.A. Knox, et al. (1985)
• Contrasting effects of alveolar macrophages and neutrophils on asbestos-induced pulmonary epithelial cell injury — D.W. Kamp, M.M. Dunn, et al. (1994)
• Morphologic characterization of alveolar macrophages from subjects with occupational exposure to inorganic particles — T. Takemura, W.N. Rom, et al. (1989)
• Stimulation of oxidant production in alveolar macrophages by pollutant and latex particles — G.E. Hatch, D.E. Gardner, et al. (1980)
• Differences between particulate and peptide stimuli on activation of oxidant production in alveolar macrophages — G.E. Hatch, A. Spock, et al. (1980)
• Alveolar macrophage stimulation of lung fibroblast growth in asbestos-induced pulmonary fibrosis — I. Lemaire, H. Beaudoin, et al. (1986)

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