Inflammatory particles stimulate thromboplastin production by human monocytes

Our plain-English summary of Inflammatory particles stimulate thromboplastin production by human monocytes, by R.T. Dean, H. Prydz (Thrombosis Research, 1983).

The study

• Authors: R.T. Dean, H. Prydz
• Journal: Thrombosis Research
• Published: 1983;30(4):357-67
• Cited by: 25 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Several inflammatory particles (zymosan, two forms of asbestos, carrageenan) and the soluble inflammatory agent dextran sulphate induced a dose- and time-dependent increase in thromboplastin activity of cultured human monocytes. Two weakly inflammatory particles (latex and anatase) had little effect. The increase largely depended on protein synthesis; was slow, reaching a peak at about 18 h; and was not due to endotoxin. This procoagulant may contribute to the fibrin deposition frequently seen in inflammatory lesions.

In plain English

This laboratory study, carried out in Oslo, Norway, tested whether particles that cause inflammation make human white blood cells called monocytes produce more thromboplastin, a substance that starts blood clotting. Monocytes from donated blood were grown in dishes, usually for 18 hours. They were exposed to zymosan (from yeast), carrageenan, dextran sulphate, chrysotile A asbestos from the UICC, a specially milled short-fibre form of the same asbestos, or the weakly inflammatory particles latex and anatase. Both asbestos preparations increased thromboplastin activity, as did zymosan, carrageenan and dextran sulphate. Latex and anatase had little effect. Detailed numbers are given mainly for zymosan: at 18 hours, activity averaged 2.7 times that of untreated cells. Blocking protein production largely reduced this increase. Further tests indicated that endotoxin contamination did not explain the zymosan effect. The long and short asbestos fibres acted similarly, which the authors said suggested that events both at the cell surface and inside the cell might contribute. The authors concluded that monocytes could contribute to clotting in infection and inflammation. The measured asbestos values are shown only in a figure that cannot be read in the text supplied.

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: Laboratory (in vitro) experiment on cultured human cells
• Who was studied: Human monocytes isolated from buffy coats (blood preparations) from single donors, cultured in dishes at the Research Institute for Internal Medicine, Rikshospitalet, Oslo, Norway; preparations were more than 95% monocytes. The total number of donors is not stated; the asbestos experiments in Fig. 3 used cells from 2 buffy coats.
• Exposure: Chrysotile A asbestos from the Union International Contre Cancer (UICC) and a specially milled short-fibre form of the same material, both heterogeneous in fibre length. Other agents tested were zymosan, carrageenan, dextran sulphate, latex, anatase and endotoxin, mostly over 18 hours of culture.
• Main results:
  • Both chrysotile A asbestos and its short-fibre form increased monocyte thromboplastin activity after 18 h, as did zymosan, carrageenan and dextran sulphate. The article states this in words, but the numerical asbestos results are shown only in Fig. 3, which cannot be read in the text supplied.
  • The weakly inflammatory particles latex and anatase had little effect. For latex at 18 h, the averaged ratio of thromboplastin activity to controls was 0.9 ± 0.4 (n=4).
  • For zymosan-treated cells, the averaged ratio of thromboplastin activity to controls was 2.7 ± 0.9 at 12 h (n=3) and 2.7 ± 0.4 at 18 h.
  • With the protein synthesis inhibitor cycloheximide, the ratio for zymosan-treated cells fell to 1.6 ± 0.06 (three experiments), compared with 2.7 ± 0.4 for zymosan alone (11 experiments). The authors described this as a 65% inhibition of the induced increase and judged the increase to depend largely on making new thromboplastin.
  • The authors reported evidence that endotoxin contamination was not responsible for the stimulation by zymosan. They also stated that zymosan, but not the other particles, was contaminated with endotoxin beyond the medium.
  • Standard UICC chrysotile, mostly fibres longer than the cells and therefore hardly taken up by them, had an effect similar to the short-fibre asbestos. The authors said this suggested that both surface and intracellular events might contribute.
  • In control and zymosan-stimulated cells at 18 h, trypsin inactivated 60-80% of the thromboplastin, which the authors took to indicate that most of it was on the cell surface.
• The authors' conclusion: The authors concluded that, in response to phagocytosis of inflammatory particles, monocytes increase thromboplastin synthesis and its transport to the cell surface. In doing so, mononuclear phagocytes could contribute to disseminated intravascular coagulation in certain infections and to extravascular coagulation in inflammation.
• Limitations the authors state:
  • Experiments with cytochalasin B were hard to interpret because of cell rounding and the difficulty of fully preventing particle uptake without toxicity. The authors therefore had no satisfactory evidence on whether taking up the particles is itself a stimulus.
  • Thromboplastin activity varied considerably between freshly isolated cell preparations.
  • Whether complement produced by the cells themselves is required was not studied.

Topics

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

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