Benign asbestos pleurisy in the rabbit. A model for the study of pathogenesis

Our plain-English summary of Benign asbestos pleurisy in the rabbit. A model for the study of pathogenesis, by B.L. Shore, C.C. Daughaday, I. Spilberg (The American Review of Respiratory Disease, 1983).

The study

• Authors: B.L. Shore, C.C. Daughaday, I. Spilberg
• Journal: The American Review of Respiratory Disease
• Published: 1983;128(3):481-5
• Cited by: 13 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Benign asbestos pleurisy is a manifestation of asbestos-induced disease that is not uncommon but often ignored. We developed an animal model to study the pathogenesis of this syndrome. Crocidolite asbestos injected into the rabbit pleural space resulted in the appearance of chemotactic activity in an exudative effusion, characterized by a polymorphonuclear leukocyte (PMN) response that peaked 4 h after the injection. The chemotactic activity and the PMN responses occurred equally in normal animals and in animals that had been depleted of complement with cobra venom. Neutropenia, induced with vinblastine, did not alter the appearance of chemotactic activity but abrogated the PMN response. Treatment with colchicine failed to block the release of chemotactic activity into the pleural fluid, but decreased the PMN response without affecting the ability of peripheral blood PMN to respond to pleural fluid chemotactic activity. When pleural fluid containing chemotactic activity was injected into the pleural space of another rabbit, a PMN response was observed. These studies suggest that the acute exudative response seen in the rabbit model of benign asbestos pleurisy results from the release of chemotactic activity from sources other than complement. The response probably depends on interaction between the asbestos and the pleural tissue. Asbestos-PMN interaction may release chemotactic factors that amplify the response secondarily. Colchicine blocked the acute response to intrapleural asbestos by a mechanism yet to be understood.

In plain English

This was an animal experiment. The authors built a rabbit model to study how benign asbestos pleurisy develops. Male New Zealand white rabbits had 5 ml of a 1% crocidolite asbestos suspension, or sterile saline, injected into the pleural space, the space around the lungs. Counts of white blood cells called PMN in the pleural fluid peaked 4 hours after injection. At 4 hours, crocidolite-injected rabbits yielded on average 124.8 million PMN (plus or minus 39.3 million), against 36.8 million (plus or minus 11.6 million) in saline-injected rabbits. Their fluid also showed more chemotactic activity, meaning it attracted these cells. The crocidolite suspension alone showed none. Removing complement, a part of the blood's immune system, with cobra venom did not significantly change the response. Blocking PMN production with vinblastine stopped PMN from entering the pleural fluid, but the chemotactic activity remained. Colchicine reduced PMN recovery but increased chemotactic activity. The authors concluded that the response was associated with chemotactic activity, and they could not explain colchicine's effect.

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 (rabbit model of benign asbestos pleurisy)
• Who was studied: Male New Zealand white rabbits weighing 2.5 to 3 kg. The total number of animals is not stated in one place. Group sizes at 4 hours were 6 crocidolite, 5 saline, 5 vinblastine-treated, 6 cobra-venom-treated and 9 colchicine-treated. The authors' department was at the Veterans Administration Medical Center and Washington University School of Medicine, St. Louis, Missouri.
• Exposure: Injection into one pleural space of 5 ml of a 1% suspension of standard UICC crocidolite asbestos (heat-treated, washed and sonicated), or of sterile saline as a control
• Main results:
  • When fluid was sampled repeatedly from the same animals, PMN recovery from the pleural fluid peaked 4 hours after injection.
  • At 4 hours, PMN recovery was 124.8 ± 39.3 million in crocidolite-injected rabbits (n = 6) versus 36.8 ± 11.6 million in saline-injected rabbits (n = 5), p less than 0.005.
  • At 4 hours, pleural fluid chemotactic activity was significantly higher in crocidolite-injected rabbits than in saline-injected rabbits: chemotactic index 11.2 ± 5.5 microns versus 2.8 ± 5.5 microns, p less than 0.01.
  • The crocidolite suspension by itself had no chemotactic activity.
  • Pleural fluid from crocidolite-injected rabbits, injected into a second group of rabbits, yielded 46 ± 10.7 million PMN after 4 hours, compared with 21 ± 3.6 million in rabbits given diluent alone.
  • In rabbits made neutropenic with vinblastine (n = 5), PMN recovery 4 hours after crocidolite was completely suppressed.
  • In the vinblastine-treated rabbits, the pleural fluid chemotactic index was not significantly different from that of rabbits with normal PMN counts (12.6 ± 3.3 versus 11.2 ± 5.5 microns).
  • In complement-depleted (cobra venom) rabbits (n = 6), PMN recovery 4 hours after crocidolite did not differ significantly from untreated rabbits: 124.8 ± 39.3 million in untreated versus 120.8 ± 30.8 million in treated.
  • In colchicine-pretreated rabbits (n = 9), PMN recovery 4 hours after crocidolite was 39.3 ± 14.3 million versus 124.8 ± 39.3 million in rabbits not pretreated, p less than 0.005.
  • Colchicine increased pleural fluid chemotactic activity: chemotactic index 19.1 ± 3.6 microns with colchicine versus 11.2 ± 5.5 microns without, p less than 0.025.
  • In PMN from 3 rabbits tested before and after colchicine, colchicine had no significant effect on the cells' ability to respond to pleural fluid chemotactic activity.
• The authors' conclusion: The authors concluded that the exudative response to intrapleural crocidolite in this model was associated with the appearance of chemotactic activity. They judged this activity probably not primarily derived from complement, possibly resulting from an interaction of pleural tissue cells with asbestos, and stated that colchicine's mechanism was yet to be understood.
• Limitations the authors state:
  • The authors could not exclude that complement factors produced locally within the pleural space contribute to the chemotactic activity.
  • The mechanism by which colchicine blocked the acute response was not understood.
  • The in vivo significance of the observed high-dose inhibition of cell migration was unclear.

Topics

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

Medical terms in this study, explained in our Lexicon: Pleurisy, Crocidolite, Neutropenia.

Related studies

• Evidence of a role for mesothelial cell-derived interleukin 8 in the pathogenesis of asbestos-induced pleurisy in rabbits — A.M. Boylan, C. Rüegg, et al. (1992)
• Pathogenesis of pleurisy, pleural fibrosis, and mesothelial proliferation — A. Herbert (1986)
• Benign asbestos pleurisy — H.B. Eisenstadt (1965)
• Ventilatory failure due to asbestos pleurisy — A. Miller, A.S. Teirstein, et al. (1983)
• Acute pleurisy in asbestos exposed persons — G.K. Sluis-Cremer, I. Webster (1972)
• Cause of Asbestos-Induced Pleurisy Forgotten — E. Böhm (2019)

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