IgG and IgA enhance the chrysotile-induced production of reactive oxygen metabolites by human polymorphonuclear leucocytes

Our plain-English summary of IgG and IgA enhance the chrysotile-induced production of reactive oxygen metabolites by human polymorphonuclear leucocytes, by M. Klockars, M. Hedenborg, J. Koistinen, et al (Clinical and Experimental Immunology, 1989).

The study

• Authors: M. Klockars, M. Hedenborg, J. Koistinen, T. Isobe
• Journal: Clinical and Experimental Immunology
• Published: 1989;78(3):372-7
• Cited by: 9 articles, as counted by NIH iCite
• Read it: PubMed · Free full text

Abstract

Chrysotile asbestos fibres induce a rapid generation of reactive oxygen metabolites by human polymorphonuclear leucocytes (PMNL) in vitro. This effect was markedly enhanced by the presence of 10-200 micrograms/ml of human gammaglobulin, purified polyclonal IgG, and monoclonal IgG and IgA myeloma proteins. Purified monoclonal IgD, IgM, kappa light chain proteins, and secretory IgA inhibited this chrysotile-induced response. No enhancing effect of IgG was observed when quartz dust or opsonized zymosan were used as stimulators of PMNL metabolism. The enhancing effect of IgG was shown to depend on opsonization of the asbestos fibre. We suggest that the IgG and IgA potentiating effect on the asbestos fibre-induced production of tissue-damaging reactive oxygen metabolites by inflammatory cells is dependent on a particle-specific binding of immunoglobulin to the fibre surface, with subsequent Fc receptor-mediated effects on cells. Such an interaction between certain immunoglobulins and asbestos may explain a number of in vivo phenomena in which immunological responses (hypergammaglobulinemia, circulating immune complexes, etc.) have been shown to relate to the progression of pulmonary asbestosis. The differences between various immunoglobulin classes and monoclonal immunoglobulins could represent an individual inflammation-modulating mechanism in the development of acute or chronic pulmonary asbestosis.

In plain English

This was a laboratory (test-tube) experiment on white blood cells (polymorphonuclear leucocytes, PMNL) from apparently healthy adults. The authors exposed the cells to a standard reference sample of chrysotile A asbestos, with and without antibodies (immunoglobulins), and measured the cells' release of reactive oxygen substances. Chrysotile at 50 micrograms per millilitre gave a mean peak light-signal reading of 31.9 mV in cells from 11 people. Adding 200 micrograms per millilitre of human gamma globulin raised this to 284.4 mV in cells from 4 people. Pooled IgG gave up to a four-fold enhancement, and all seven IgA proteins tested also enhanced the response. Monoclonal IgM, IgD, light-chain proteins and secretory IgA inhibited it. IgG did not enhance the response to quartz dust or to serum-opsonized zymosan. Coating the fibres with IgG beforehand produced the enhancement, but pre-treating the cells did not. The authors concluded that IgG and IgA strongly enhance this response. Assuming these oxygen products play a role in asbestosis, they suggested antibody differences could partly explain why only some exposed workers develop it; this was not tested in workers.

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 human white blood cells (polymorphonuclear leucocytes)
• Who was studied: Polymorphonuclear leucocytes isolated from venous blood of apparently healthy adults (cells from 3 to 11 individuals per experiment); Helsinki, Finland
• Exposure: UICC standard reference chrysotile A asbestos (mostly 50 micrograms per millilitre), alone and combined with human gamma globulin, pooled polyclonal IgG, monoclonal IgG, IgA, IgM and IgD myeloma proteins, light-chain proteins and secretory IgA; quartz dust and opsonized zymosan were used as comparison stimuli
• Main results:
  • Superoxide production by PMNL was enhanced up to five-fold when 200 to 400 micrograms per millilitre of pooled IgG was present together with chrysotile
  • Chrysotile alone (50 micrograms per millilitre) gave a peak chemiluminescence of 31.9 plus or minus 12.2 mV (mean plus or minus s.d., n = 11)
  • Chrysotile plus 200 micrograms per millilitre human gamma globulin gave 284.4 plus or minus 84.6 mV in cells from 4 individuals. The text states this was significantly above the sum of the separate responses (P less than 0.005)
  • Pooled IgG at 100 to 200 micrograms per millilitre with chrysotile gave an up to four-fold, dose-dependent enhancement (P less than 0.01)
  • Pooled IgG had no enhancing effect when quartz dust or serum-opsonized zymosan were the stimulus (data not shown)
  • Monoclonal IgG increased the chrysotile response in a dose-dependent way, while two light-chain proteins inhibited it
  • All seven IgA myeloma proteins enhanced the chrysotile-induced response compared with the sum of the separate responses (P less than 0.01)
  • Monoclonal IgM, IgD and secretory IgA at 100 micrograms per millilitre inhibited the chrysotile response (P less than 0.01 for secretory IgA)
  • Fibres pre-coated with pooled IgG gave a response similar to fibres plus IgG, while pre-incubating the cells with IgG gave no enhancement
• The authors' conclusion: The authors concluded that soluble IgG and IgA are potent enhancers of reactive oxygen production by chrysotile-exposed PMNL in vitro. They suggested that differences between antibody types could partly explain why only a fraction of exposed workers develop asbestosis, assuming these oxygen products play a role in the disease.

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, Monoclonal, Myeloma, Asbestosis, Inflammation.

Related studies

• Production of reactive oxygen metabolites induced by asbestos fibres in human polymorphonuclear leucocytes — M. Hedenborg, M. Klockars (1987)
• Chemiluminescent detection of induced reactive oxygen metabolite production of human polymorphonuclear leucocytes by anthophyllite asbestos — T. Iwata, N. Kohyama, et al. (2002)
• Cellular mechanisms of reactive oxygen metabolite generation from human polymorphonuclear leukocytes induced by crocidolite asbestos — T. Ishizaki, E. Yano, et al. (1997)
• Crocidolite-induced reactive oxygen metabolites generation from human polymorphonuclear leukocytes — T. Ishizaki, E. Yano, et al. (1994)
• Production of reactive oxygen species by man-made vitreous fibres in human polymorphonuclear leukocytes — M. Ruotsalainen, M.R. Hirvonen, et al. (1999)
• Measurement of reactive oxygen metabolites produced by human monocyte-derived macrophages exposed to mineral dusts — P. Nyberg, M. Klockars (1990)

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