Asbestos-activated peritoneal macrophages release a factor(s) which inhibits lymphocyte mitogenesis

Our plain-English summary of Asbestos-activated peritoneal macrophages release a factor(s) which inhibits lymphocyte mitogenesis, by K. Donaldson, J.M. Davis, K. James (Environmental Research, 1984).

The study

• Authors: K. Donaldson, J.M. Davis, K. James
• Journal: Environmental Research
• Published: 1984;35(1):104-14
• Cited by: 6 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Intraperitoneal asbestos injection in mice has previously been reported to elicit an activated macrophage population. In the present study supernatants from such macrophages were tested for their effect on thymocyte mitogenesis in response to concanavalin A; control supernatants were obtained from saline- and latex-elicited macrophages. Supernatants from asbestos-elicited macrophages were significantly inhibitory to thymocyte mitogenesis while saline- and latex-elicited macrophages did not release significant amounts of such activity. Asbestos-activated macrophage supernatants were inhibitory in a dose-dependent way and the activity was not secreted by macrophages from mice which had received asbestos in the long term. The inhibitory activity was partially dialysable. Supernatants prepared by treating macrophages in vitro with a lethal dose of asbestos were not inhibitory suggesting that the inhibitory activity in the supernatants of asbestos-activated macrophages did not leak from dead or dying cells. The asbestos macrophage supernatant was also significantly inhibitory to mature T-cell-enriched spleen cells but had no effect on fibroblasts, suggesting that the inhibitory effect could be lymphoid cell specific.

In plain English

This was a laboratory study in mice. The authors injected CBA/Ca mice in the abdominal (peritoneal) cavity with 2.5 mg of UICC chrysotile asbestos, latex beads, or saline. Three days later they collected peritoneal macrophages (scavenger cells). They then tested the fluid these cells were cultured in on how mouse thymus cells (thymocytes) grew when stimulated with concanavalin A. Measured as raw counts, no differences were significant. Measured as a ratio against stimulated cells within each experiment, fluid from chrysotile-elicited macrophages significantly reduced thymocyte growth, with ratios of 0.59 and 0.65 at the two stimulant doses. Saline and latex fluids were not significantly suppressive. The effect was dose-related and was reduced but not removed by dialysis. It was absent in fluid from macrophages taken 280 days after injection. It was also absent in fluid from macrophages given a chrysotile dose in the dish that killed 70% of them. Chrysotile fluid also inhibited T-cell-enriched spleen cells, but did not significantly inhibit fibroblasts. The authors concluded the factor appeared to be actively secreted. They noted their peritoneal model differs from lung (alveolar) macrophages.

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: Animal experiment (mice injected intraperitoneally) with laboratory (in vitro) cell-growth assays
• Who was studied: CBA/Ca mice bred at the University of Edinburgh, 12-16 weeks old at the start; thymocytes from 3- to 6-week-old mice; numbers of mice not stated
• Exposure: A single intraperitoneal injection of 2.5 mg UICC chrysotile asbestos, compared with latex beads or saline (Dulbecco A). Macrophages were collected 3 days or 280 days after injection. Separately, control macrophages were treated with chrysotile in vitro for 48 hours, which killed 70% of them.
• Main results:
  • Measured as raw thymidine uptake counts, there were no significant differences between groups.
  • Expressed as a mitogenic index, chrysotile macrophage fluid significantly suppressed thymocyte growth compared with saline macrophage fluid: P < 0.02 at 1 microgram/ml concanavalin A and P < 0.05 at 2 micrograms/ml.
  • Mitogenic index with chrysotile macrophage fluid was 0.59 (SD 0.14) at 1 microgram/ml and 0.65 (SD 0.16) at 2 micrograms/ml concanavalin A.
  • Fluids from saline- and latex-elicited macrophages were not significantly suppressive.
  • Inhibition was dose-related; it was significant with 50% chrysotile macrophage fluid at both stimulant doses.
  • Fluid from macrophages taken 280 days after chrysotile injection was not inhibitory.
  • Control macrophages were treated in vitro with 500 micrograms chrysotile per ml for 48 hours, which killed 70% of them. Fluid from this culture was not inhibitory.
  • Dialysis reduced the inhibitory activity, but significant inhibition remained at 2 micrograms/ml concanavalin A.
  • Chrysotile macrophage fluid significantly inhibited growth of T-cell-enriched spleen cells compared with saline fluid (P < 0.05 at both doses).
  • Chrysotile macrophage fluid did not significantly inhibit fibroblast growth.
• The authors' conclusion: The authors concluded that the inhibitory factor is not leaking from dead or damaged cells but is actively secreted by activated macrophages.
• Limitations the authors state:
  • The study used peritoneal macrophages, whereas the authors regard alveolar (lung) macrophages as the ideal cell for studying asbestos effects.

Topics

Medical terms in this study, explained in our Lexicon: Macrophage, Fibroblast.

Related studies

• Secretion of fibronectin by mineral dust-derived alveolar macrophages and activated peritoneal macrophages — R. Davies, G. Erdogdu (1989)
• Activated alveolar macrophages express the insulin-like growth factor-I receptor — W.N. Rom, P. Pääkkö (1991)
• Cytotoxic effect of asbestos on macrophages in different activation states — A. Wright, K. Donaldson, et al. (1983)
• Interactions of asbestos-activated macrophages with an experimental fibrosarcoma — K. Donaldson, J.M. Davis, et al. (1983)
• Characteristics of peritoneal macrophages induced by asbestos injection — K. Donaldson, J.M. Davis, et al. (1982)
• Carborundum pneumoconiosis. Fibers in the mineral activate macrophages to produce fibroblast growth factors and sustain the chronic inflammatory disease — R. Bégin, A. Dufresne, et al. (1989)

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