Superoxide anion release by alveolar macrophages exposed to respirable industrial fibres: modifying effect of fibre opsonisation

Our plain-English summary of Superoxide anion release by alveolar macrophages exposed to respirable industrial fibres: modifying effect of fibre opsonisation, by K. Donaldson, I.M. Hill, P.H. Beswick (Experimental and Toxicologic Pathology, 1995).

The study

• Authors: K. Donaldson, I.M. Hill, P.H. Beswick
• Journal: Experimental and Toxicologic Pathology
• Published: 1995;47(4):229-31
• Cited by: 14 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Phagocyte-derived free radicals are considered to play a role in fibre-related pathology and the components of the lung lining fluid could modify the surface of fibres. Therefore we examined the ability of long amosite asbestos and a range of man-made fibres to stimulate release of superoxide anion from rat alveolar macrophages when they were in their native form (unopsonised) and opsonised by incubation in rat Immunoglobulin G. We also assessed the specific amount of opsonin adsorbed to each fibre type. In the uncoated form all of the fibres produced modest amounts of superoxide release from macrophages. When they were opsonised however there was an effect on stimulation of release of superoxide that was fibre-specific. Both MMVF21 and RCF 1 were dramatically enhanced in their ability to stimulate release and this was related to a high affinity of their surface for IgG. Code 100/475 and SiC were not substantially affected by opsonisation and this was reflected in their low affinity for IgG. Long amosite had low affinity for IgG but showed dramatic enhancement of capacity to stimulate superoxide release. These fibre-specific differences in the effect of a coating of material that is found in the lung lining points out the problems of interpretation of in vitro data and more work on this important area is warranted.

In plain English

This was a laboratory study using alveolar macrophages, a type of immune cell taken from the lungs of rats. The authors tested whether five kinds of fibres made these cells release superoxide anion, a reactive form of oxygen. The fibres were long amosite asbestos and four man-made fibres: refractory ceramic fibre 1 (RCF1), man-made vitreous fibre 21 (MMVF21), Code 100/475 glass microfibre and silicon carbide. Each fibre was tested uncoated and after being coated (opsonised) with rat immunoglobulin G (IgG), a protein found in lung lining fluid. Results were reported for a dose of 3 million fibres. The authors also measured how much IgG stuck to each fibre. Uncoated, all fibres caused modest superoxide release. Coating substantially increased release for amosite, MMVF21 and RCF1, but not much for Code 100/475 or silicon carbide. MMVF21 and RCF1 bound the most IgG. Amosite bound little IgG yet was much more active than its IgG binding predicted. The authors concluded that these fibre-specific differences show the problems of interpreting in vitro data.

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: In vitro laboratory experiment: fibres were tested uncoated and after coating (opsonisation) with rat immunoglobulin G, with saline-treated control fibres
• Who was studied: Rat alveolar macrophages (lung immune cells); the number of animals is not given
• Exposure: Long amosite asbestos, refractory ceramic fibre 1 (RCF1), man-made vitreous fibre 21 (MMVF21), Code 100/475 glass microfibre and silicon carbide, each uncoated or opsonised with rat IgG; results shown for a single dose of 3 million fibres
• Main results:
  • Uncoated (unopsonised), all five fibre types caused modest superoxide release from the macrophages
  • After opsonisation, amosite, MMVF21 and RCF1 all caused substantially more superoxide release
  • Code 100/475 and silicon carbide were not substantially affected by opsonisation
  • MMVF21 and RCF showed the greatest binding (affinity) for IgG
  • Superoxide release tracked the amount of IgG bound, except for long amosite, which was more active than its IgG binding would predict
• The authors' conclusion: The authors concluded that fibre-specific differences in the effect of a coating found in the lung lining point out problems in interpreting in vitro data, and that more work is warranted
• Limitations the authors state:
  • The authors note that how much opsonisation enhanced each fibre's activity did not simply correlate with the fibres' harmfulness (pathogenicity) in animal studies
  • The authors note that lung lining fluid is complex, with many components likely competing to bind the fibre surface, which this study did not reproduce and which needs further investigation

Topics

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

Medical terms in this study, explained in our Lexicon: Superoxide, Alveolar Macrophage, Pathology, Lung Lining Fluid, Amosite, Macrophage.

Related studies

• Differential release of superoxide anions by macrophages treated with long and short fibre amosite asbestos is a consequence of differential affinity for opsonin — I.M. Hill, P.H. Beswick, et al. (1995)
• Enhancement of the macrophage oxidative burst by immunoglobulin coating of respirable fibers: fiber-specific differences between asbestos and man-made fibers — I.M. Hill, P.H. Beswick, et al. (1996)
• IgG specifically enhances chrysotile asbestos-stimulated superoxide anion production by the alveolar macrophage — R.K. Scheule, A. Holian (1989)
• In vitro activity of silicon carbide whiskers in comparison to other industrial fibers using four cell culture systems — N.F. Johnson, M.D. Hoover, et al. (1992)
• Dehydroepiandrosterone inhibits the spontaneous release of superoxide radical by alveolar macrophages in vitro in asbestosis — W.N. Rom, T. Harkin (1991)
• Toxicity in vitro of some silicon carbides and silicon nitrides: whiskers and powders — I. Svensson, E. Artursson, et al. (1997)

Browse more research in Experimental and Toxicologic Pathology, or return to medical research.