Effects of chrysotile asbestos on mononuclear cells in vitro

Our plain-English summary of Effects of chrysotile asbestos on mononuclear cells in vitro, by S. Kagamimori, M.P. Scott, D.G. Brown, et al (British Journal of Experimental Pathology, 1980).

The study

• Authors: S. Kagamimori, M.P. Scott, D.G. Brown, R.E. Edwards, M.M. Wagner
• Journal: British Journal of Experimental Pathology
• Published: 1980;61(1):55-60
• Cited by: 13 articles, as counted by NIH iCite
• Read it: PubMed · Free full text

Abstract

Chrysotile asbestos (400 micrograms/ml) was not found to be cytotoxic towards human blood lymphocytes in culture over a 72 h period, although there was indirect evidence of cytoxicity towards plastic adherent mononuclear cells (PAM). There was significant suppression of 3H-thymidine incorporation into cells cultured with phytohaemagglutinin (PHA) in the presence of fibres. It was found even when chrysotile was added 24 h after PHA. No suppression was found for chrysotile-treated PAM-depleted cultures in comparison to control cultures. Antibody-dependent cell-mediated cytotoxicty (ADCC) was inhibited by the presence of chrysotile, and appeared to be due to prevention of contact between antibody-coated target cells and effector cells.

In plain English

This laboratory study, from the Medical Research Council Pneumoconiosis Unit in Wales, exposed cultured human blood cells to chrysotile asbestos (Canadian chrysotile B, a UICC standard sample). The blood came from patients awaiting minor surgery or from healthy laboratory volunteers. At 400 micrograms per millilitre, chrysotile did not significantly change cell survival over 72 hours. This held both for the whole mononuclear cell mixture and with the plastic-adherent cells (monocytes) removed. A comparison between the two was the authors' indirect evidence that monocytes were killed preferentially. Chrysotile significantly reduced the cells' growth response to the stimulant phytohaemagglutinin (PHA), even when added 24 hours after it. Once monocytes were removed, this reduction appeared at only one PHA dose and not in the timed experiments. In a test of antibody-dependent cell killing, chrysotile at 3 and 5 micrograms per millilitre reduced killing of antibody-coated target cells when added before the killer cells. The authors suggested that chrysotile reduced the PHA response mainly by damaging monocytes, and that it might reduce cell killing by blocking contact between target and killer cells.

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 peripheral blood mononuclear cells (PBMC) in culture
• Who was studied: Human blood cells from preoperative minor-surgery patients or healthy laboratory volunteers, studied at the MRC Pneumoconiosis Unit, Llandough Hospital, Penarth, Wales. Donor numbers: viability tests 24 donors (12 for PBMC, 12 for PAM-depleted cells); PHA tests 12 donors; PAM-depleted PHA tests another 7 donors; 7 different donors for each of the 3 antibody-dependent cytotoxicity experiments.
• Exposure: Canadian chrysotile B (UICC standard sample), added to cultures at a final concentration of 400 micrograms per ml. Concentrations up to 5 micrograms per ml were used in the antibody-dependent cytotoxicity tests.
• Main results:
  • Viability of PBMC did not differ significantly between control and chrysotile-treated cultures at 24, 48 or 72 h. The same was true for PAM-depleted PBMC.
  • Chrysotile-treated PBMC had significantly lower viability than untreated PAM-depleted PBMC. The authors took this as suggesting preferential killing of monocytes.
  • When PHA and chrysotile were added together, 3H-thymidine uptake was significantly lower in chrysotile-exposed PBMC at each of the 3 PHA concentrations. In PAM-depleted PBMC, the difference was significant only at 0.5 micrograms per 2 ml of culture.
  • In PBMC, 3H-thymidine incorporation was significantly depressed whether chrysotile was added 0, 6 or 24 h after PHA, with greater significance at 0 and 6 h. This effect was not found in PAM-depleted PBMC.
  • Antibody-coated Chang cells plus effector cells released significantly less 51Cr when chrysotile (3 and 5 micrograms per ml) was added before the effector cells, compared with unexposed controls. In contrast, Chang cells alone, or without antibody but with effector cells, released more 51Cr in the presence of chrysotile at those levels.
• The authors' conclusion: The authors suggested that chrysotile interferes with 3H-thymidine incorporation mainly by damaging monocytes rather than by blocking PHA binding. They also suggested that inhibition of antibody-dependent cell killing might be due to blocking of contact between antibody-coated target cells and effector cells. They proposed that lymphocyte-monocyte cooperation may be lost in vivo in the presence of asbestos fibres.
• Limitations the authors state:
  • The authors described the evidence that chrysotile is toxic to plastic adherent mononuclear cells as indirect.
  • Only one fibre type was tested. The authors said the mechanism of ADCC inhibition could be clarified by testing fibres of varying sizes and other asbestos types.

Topics

Medical terms in this study, explained in our Lexicon: Chrysotile.

Related studies

• In vitro depression of human lymphocyte mitogen response (phytohaemagglutinin) by asbestos fibres — R.G. Barbers, W.W. Shih, et al. (1982)
• Sequential immunological studies in an asbestos-exposed population. II. Factors affecting lymphocyte function — M.J. Campbell, M.M. Wagner, et al. (1980)
• Chromosomal aberrations induced by chrysotile and crocidolite in human lymphocytes in vitro — F. Valerio, M. de Ferrari, et al. (1983)
• Activation of human CD4+CD45RA+ T cells by chrysotile asbestos in vitro — K. Kinugawa, A. Ueki, et al. (1992)
• Prognostic significance of the lymphocyte-to-monocyte ratio in patients with malignant pleural mesothelioma — T. Yamagishi, N. Fujimoto, et al. (2015)
• Prognostic value of the lymphocyte-to-monocyte ratio and other inflammatory markers in malignant pleural mesothelioma — A.C. Tanrikulu, A. Abakay, et al. (2016)

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