Pathogenesis of pleural plaques

Our plain-English summary of Pathogenesis of pleural plaques, by J.A. Elias, M.D. Rossman, R.P. Daniele (The American Review of Respiratory Disease, 1985).

The study

• Authors: J.A. Elias, M.D. Rossman, R.P. Daniele
• Journal: The American Review of Respiratory Disease
• Published: 1985;131(6):965-6
• Type of article: Letter
• Cited by: 1 article, as counted by NIH iCite
• Read it: PubMed · Publisher
• In J-M's library: Johns-Manville's company medical library held a copy (J-M no. 001211).

In plain English

This is a short letter to the editor, not a new study, and the authors reported no new data. It commented on an earlier experiment by Sahn and Anthony in which asbestos was put into the pleural space (the space between the membranes covering the lungs and lining the chest wall) of rabbits. As the letter describes that experiment, normal rabbits and neutropenic rabbits (rabbits short of a type of white blood cell) reacted differently. The normal rabbits developed discrete pleural plaques. The neutropenic rabbits, which did not show an influx of macrophages into the pleural space, developed diffuse pleural fibrosis. The letter does not name the asbestos fiber type. The authors offered what they called a speculation about why. They noted that laboratory studies have shown that lung and blood immune cells can both inhibit and stimulate the growth and collagen production of fibroblasts, the cells that make scar tissue. They suggested that macrophages and lymphocytes entering the pleural space in normal rabbits may hold back scarring and so help produce discrete plaques. They suggested that the diffuse fibrosis in the other animals might result in part from the absence of this restraint.

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: Letter to the editor (correspondence) offering a hypothesis about another group's published animal experiment; no new data
• Who was studied: No subjects of its own. The letter comments on Sahn and Anthony's study of normal and neutropenic rabbits; the neutropenic rabbits did not have a macrophage influx into the pleural space
• Exposure: Asbestos placed in the pleural space of rabbits (intrapleural asbestos) in the study being discussed; fiber type not stated in this letter
• The authors' conclusion: The authors proposed that macrophages and lymphocytes entering the pleural space in normal rabbits may inhibit the pleural fibrotic process and so be important in forming discrete pleural plaques. They proposed that diffuse fibrosis in animals without this influx of immune cells might result in part from the absence of this inhibition. They based this on earlier laboratory (in vitro) findings that lung and blood immune cells can inhibit as well as stimulate fibroblast growth and collagen production.
• Limitations the authors state:
  • The authors present their explanation as speculation, not as a tested finding

Topics

The National Library of Medicine indexes this study under subjects our site covers: Pleural plaques and thickening.

Medical terms in this study, explained in our Lexicon: Pleural Plaques.

Related studies

• Pathogenesis of pleural fibrosis — S.E. Mutsaers, C.M. Prele, et al. (2004)
• Asbestosis, pleural plaques and diffuse pleural thickening: three distinct benign responses to asbestos exposure — P.A. Gevenois, V. de Maertelaer, et al. (1998)
• Pleural plaques and asbestosis: dose- and time-response relationships based on HRCT data — C. Paris, S. Thierry, et al. (2009)
• Asbestos-related pleural plaques and lung function — L.C. Oliver, E.A. Eisen, et al. (1988)
• Subpleural fat pads in patients exposed to asbestos: distinction from non-calcified pleural plaques — E.N. Sargent, W.D. Boswell, et al. (1984)
• Aetiology of pleural plaques — V. Rous, J. Studený (1970)

Browse more research in The American Review of Respiratory Disease, or return to medical research.