The chemiluminescent response of human phagocytic cells to mineral dusts

Our plain-English summary of The chemiluminescent response of human phagocytic cells to mineral dusts, by I.P. Gormley, M.J. Kowolik, R.T. Cullen (British Journal of Experimental Pathology, 1985).

The study

• Authors: I.P. Gormley, M.J. Kowolik, R.T. Cullen
• Journal: British Journal of Experimental Pathology
• Published: 1985;66(4):409-16
• Cited by: 27 articles, as counted by NIH iCite
• Read it: PubMed · Free full text

Abstract

Luminol-dependent chemiluminescence (CL) was used to assess the in vitro production of reactive oxygen species by human neutrophils and monocytes on exposure to six standard respirable mineral dusts. Every dust caused CL production in both phagocytic cell types, although, for each dust, the two cells showed a different pattern of response. Light output was markedly affected by the presence of serum in the system. While the results illustrated the complexity of the interaction between mineral dusts and monocytes and neutrophils, they did not support the hypothesis that pathogenic dusts would induce the production of more reactive oxygen species than non-pathogenic dusts.

In plain English

This laboratory study used cells, not people. The authors used a light-based test (luminol-dependent chemiluminescence), an indirect measure of reactive oxygen species production, on two kinds of human white blood cells, neutrophils and monocytes. All cells came from one healthy adult male donor. The cells were exposed to six dusts: UICC crocidolite and chrysotile A asbestos, two clays (kaolinite KGa-1 and montmorillonite STx-1), quartz DQ12, and titanium dioxide, which the authors describe as generally considered of very low toxicity. Results were expressed as a percentage of the response to zymosan, a standard stimulant. Every dust produced some response in both cell types. In neutrophils, both asbestos samples gave low peaks: 4% with serum, and 6% for crocidolite and 7% for chrysotile without serum. In monocytes, chrysotile peaked at 70% with serum and 35% without, and crocidolite at 28.0% and 26.0%. In monocytes, titanium dioxide produced more than quartz. The authors concluded that the results cast doubt on the idea that disease-causing dusts induce cells to release more reactive oxygen species than non-disease-causing dusts, though the responses might still matter in the body.

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 measuring luminol-dependent chemiluminescence (an indirect measure of reactive oxygen species production) from human blood cells exposed to dusts; results are from single dose-response experiments
• Who was studied: Neutrophils and monocytes separated from the blood of a single healthy adult male donor, Edinburgh (Institute of Occupational Medicine and University of Edinburgh); no human health outcomes were studied
• Exposure: Six standard respirable dusts: UICC crocidolite, UICC chrysotile A, kaolinite clay KGa-1, montmorillonite clay STx-1, quartz DQ12 and titanium dioxide (rutile). Doubling dilutions gave final concentrations up to 3 mg/ml. Dusts were added with or without prior coating (opsonization) with 10% human AB serum.
• Main results:
  • Neutrophils, dusts coated with serum: both asbestos samples gave only minimal responses (peak 4.0% of the zymosan control for both crocidolite and chrysotile). The highest response was 25% for STx-1 at 3.0 mg/ml.
  • Neutrophils, dusts without serum: asbestos responses were again low (crocidolite 6.0%, chrysotile 7.0%). The clays gave marked responses: STx-1 114% and KGa-1 67%.
  • Monocytes, dusts coated with serum: chrysotile produced 70% of the zymosan control and crocidolite 28.0% (Table 1). STx-1 produced 16% and titanium dioxide 80.0%.
  • Monocytes, dusts without serum: responses were generally low, and the maximum was 35% of control, with chrysotile. Crocidolite produced 26.0% (Table 2).
  • The response depended on cell type and on serum coating. Neutrophils generally responded more to uncoated dusts, and monocytes more to coated dusts.
  • Titanium dioxide, described as an 'inert' dust, induced more chemiluminescence than quartz in monocytes (with or without serum) and in neutrophils with serum.
  • Ranking the dusts by how many cells they killed (trypan blue test) did not match their chemiluminescence levels.
  • In most cases the dusts did not draw out the cells' full chemiluminescence capacity. Adding zymosan afterwards produced further light output, including after chrysotile and crocidolite exposure of neutrophils.
• The authors' conclusion: The authors concluded that the results appear to cast doubt on the idea that disease-causing mineral dusts induce greater release of reactive oxygen species than non-disease-causing dusts. They added that the chemiluminescence all dusts caused may still be of importance in the more complex situation in the body, and that further work is required.
• Limitations the authors state:
  • The number of particles interacting with the cell membrane, known to matter, was not assessed because the dusts differed widely in physical nature.
  • Only a small number of samples was tested, so no relationship with particle size could be expected to show.
  • Direct evidence of the fibrogenic potential of the specific dusts used was not available.
  • Human blood monocytes are much less activated than lung (alveolar) macrophages, which the authors offer as a possible reason why their results differed from a guinea-pig study.

Topics

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

Medical terms in this study, explained in our Lexicon: Reactive Oxygen Species (ROS).

Related studies

• Measurement of reactive oxygen metabolites produced by human monocyte-derived macrophages exposed to mineral dusts — P. Nyberg, M. Klockars (1990)
• Polyvinylpyridine-N-oxide and carboxymethyl cellulose inhibit mineral dust-induced production of reactive oxygen species by human macrophages — P. Nyberg (1991)
• Increased mineral dust-induced production of reactive oxygen species by blood monocytes from patients with malignant diseases — P.W. Nyberg, S.A. Nordman, et al. (1994)
• The ability of mineral dusts and fibres to initiate lipid peroxidation. Part I: parameters which determine this ability — M. Gulumian (1999)
• Interleukin 1 production and accessory cell function of rat alveolar macrophages exposed to mineral dust particles — Y. Oghiso, Y. Kubota (1987)
• Production of reactive oxygen metabolites induced by asbestos fibres in human polymorphonuclear leucocytes — M. Hedenborg, M. Klockars (1987)

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