IgG specifically enhances chrysotile asbestos-stimulated superoxide anion production by the alveolar macrophage

Our plain-English summary of IgG specifically enhances chrysotile asbestos-stimulated superoxide anion production by the alveolar macrophage, by R.K. Scheule, A. Holian (American Journal of Respiratory Cell and Molecular Biology, 1989).

The study

• Authors: R.K. Scheule, A. Holian
• Journal: American Journal of Respiratory Cell and Molecular Biology
• Published: 1989;1(4):313-8
• Cited by: 24 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

The interaction of chrysotile asbestos with alveolar macrophages in vitro is known to stimulate cellular superoxide anion production. However, it is likely that particulates in the respiratory tract are present together with components of the pulmonary surfactant, and it is not known how these components may alter the bioactivity of the particulate. We now show that guinea pig immunoglobulin G, a surfactant protein, causes a significant, dose-dependent enhancement of superoxide anion production by nonadherent guinea pig alveolar macrophages in response to chrysotile asbestos. This enhancement could not be mimicked by other particulates or proteins, including IgG fragments, implying that the interaction between IgG, cell, and chrysotile is relatively specific. The enhancing effect of IgG in solution could be reproduced by pretreating the chrysotile asbestos with IgG. The fact that IgG specifically enhances chrysotile asbestos-stimulated superoxide anion production, in turn, leads to a proposal for a molecular mechanism by which asbestos may stimulate the guinea pig macrophage, namely, by crosslinking cell-surface immunoglobulin Fc receptors. In view of the submicromolar concentrations at which IgG was effective in enhancing macrophage stimulation by chrysotile asbestos in vitro, these results also suggest that IgG adsorption may play a role in the progression of asbestos-induced pulmonary fibrosis.

In plain English

This was a laboratory experiment on lung immune cells (alveolar macrophages) taken from guinea pigs, not a study of people. The authors tested whether guinea pig immunoglobulin G (IgG), an antibody protein, changes the cells' release of superoxide anion, a reactive form of oxygen, when the cells meet chrysotile asbestos in a dish. IgG increased the response to chrysotile in a dose-dependent way, with half the maximum effect at approximately 6 micrograms per ml (40 nM). Six other proteins, and two fragments of IgG, did not significantly change the response. IgG did not significantly enhance the response to crocidolite asbestos, silica, talc, aluminum or latex beads. Chrysotile gave the largest response, and IgG enhanced it about 2-fold. Coating chrysotile with IgG beforehand gave a similar increase, while pre-treating the cells gave about the same result as untreated cells. The authors suggested that IgG coating may play a role in the progression of asbestos-induced pulmonary fibrosis, but noted that a role in living lungs remains to be shown.

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 on isolated animal cells
• Who was studied: Purified alveolar macrophages from guinea pigs (number of animals not stated); cell viabilities typically greater than 93% and purity greater than 93% alveolar macrophages
• Exposure: Chrysotile asbestos (Calidria asbestos, RG-144, from Union Carbide), milled and sized to 1 to 5 micrometres, used at 25 micrograms per ml with or without guinea pig IgG. Comparison particles were crocidolite asbestos, silica, talc, aluminum microspheres and latex beads. Comparison proteins were aldolase, albumin, fibrinogen, myoglobin, ribonuclease, transferrin, and the IgG fragments Fc and F(ab')2.
• Main results:
  • With chrysotile, adding IgG increased the macrophages' superoxide anion production in a dose-dependent, saturable way, with half-maximal enhancement at approximately 6 micrograms IgG per ml (40 nM)
  • At identical molar concentrations, six other proteins had no significant effect on chrysotile-stimulated superoxide anion production
  • The Fc and F(ab')2 fragments of IgG, at concentrations equivalent to intact IgG, did not significantly affect chrysotile-stimulated superoxide anion production
  • Of all particles examined, chrysotile asbestos elicited the largest response, and IgG enhanced this response about 2-fold. IgG did not significantly enhance responses to silica, crocidolite asbestos, talc, latex beads or aluminum.
  • Chrysotile pretreated with IgG and then washed gave enhanced superoxide production similar to adding chrysotile to cells in the presence of IgG
  • Macrophages pretreated with IgG and washed produced virtually the same amount of superoxide anion as untreated control cells
• The authors' conclusion: The authors concluded that their results suggest that IgG adsorption may play a role in the progression of asbestos-induced pulmonary fibrosis
• Limitations the authors state:
  • Whether the role of IgG shown in vitro applies in living lungs remains to be shown
  • The results do not show whether the enhancement comes from better binding of particles to cells, greater stimulation of the cells, or both

Mines named here

Asbestos mines this study is about. Each mine's page says who ran it, when it worked, and what it produced.

• Santa Rita mine, Joaquin Ridge near Coalinga, California

All asbestos mines

Topics

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

Medical terms in this study, explained in our Lexicon: Chrysotile, Superoxide, Alveolar Macrophage, Macrophage, Pulmonary Fibrosis.

Related studies

• Superoxide anion release by alveolar macrophages exposed to respirable industrial fibres: modifying effect of fibre opsonisation — K. Donaldson, I.M. Hill, et al. (1995)
• 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)
• Asbestos effects on superoxide production. An in vitro study of hamster alveolar macrophages — B.W. Case, M.P. Ip, et al. (1986)
• IgG and IgA enhance the chrysotile-induced production of reactive oxygen metabolites by human polymorphonuclear leucocytes — M. Klockars, M. Hedenborg, et al. (1989)
• Dehydroepiandrosterone inhibits the spontaneous release of superoxide radical by alveolar macrophages in vitro in asbestosis — W.N. Rom, T. Harkin (1991)
• Phospholipase A2-mediated superoxide production of murine peritoneal macrophages induced by chrysotile stimulation — T. Nakajima, M. Ito, et al. (2000)

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