The mesothelial cell and its role in asbestos-induced pleural injury

Our plain-English summary of The mesothelial cell and its role in asbestos-induced pleural injury, by M. Kuwahara, E. Kagan (International Journal of Experimental Pathology, 1995).

The study

• Authors: M. Kuwahara, E. Kagan
• Journal: International Journal of Experimental Pathology
• Published: 1995;76(3):163-70
• Type of article: Review
• Cited by: 17 articles, as counted by NIH iCite
• Read it: PubMed · Free full text

Summary of the article

This review examined the role of the pleural mesothelial cell in the pleura's response to injury, with emphasis on possible mechanisms of asbestos-induced pleural fibrosis and diffuse malignant mesothelioma. The authors noted that pleural fibrosis is the most common manifestation of human asbestos-induced disease but that its pathogenesis is poorly understood. They summarised published human, animal and cell-culture studies on pleural anatomy and on the capacity of cultured mesothelial cells to produce cytokines, extracellular matrix components, procoagulant and fibrinolytic factors, and fibroblast chemoattractants and growth factors. They then reviewed evidence on asbestos specifically. Mesothelial cells took up asbestos fibres. Fibres translocated to the pleura, with shorter chrysotile fibrils reported in parietal pleura and plaques. Fibres induced secretion of interleukin-8 and fibronectin, increased collagen synthesis and pleural macrophage recruitment, and caused oxidant injury and activation of the c-fos and c-jun protooncogenes. The authors observed that a neutrophil-driven mechanism lacked clinical foundation, because benign asbestos effusions are rare and most people with plaques have no history of effusion. They also stated that no studies of asbestos and nitric oxide in mesothelial cells were known to them. They proposed a hypothetical scheme in which the mesothelial cell is the key effector cell and the pleural macrophage an important secondary participant. In this scheme, uptake of fibres that have reached the pleura starts a protracted process, which they suggested may explain the location and long latency of the lesions.

PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

In plain English

This article was a review, not a new study. The authors summarized published research, mostly laboratory work on cultured human, rabbit and rat pleural mesothelial cells (the cells lining the chest cavity) and animal experiments, to consider how asbestos might injure the pleura. They described earlier studies reporting that inhaled asbestos fibres can reach the pleura, and that only shorter chrysotile fibrils appeared to favour the parietal pleura and pleural plaques. Other cited studies reported that asbestos fibres stimulated cultured mesothelial cells to release interleukin-8 and fibronectin and to make more collagen. Further cited studies linked crocidolite and chrysotile to oxidant stress responses and to activation of the c-fos and c-jun genes in these cells. The authors wrote that very little is known about how asbestos-related pleural fibrosis and diffuse malignant mesothelioma develop. As a hypothesis, they proposed that the pleural mesothelial cell is the key effector cell in asbestos-induced pleural fibrosis and that the pleural macrophage is an important secondary participant. They noted that fibre uptake by mesothelial cells in living animals still awaited confirmation in humans.

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: Narrative review ("Current Status Review") of published laboratory, animal and clinical studies on the pleural mesothelial cell and asbestos-induced pleural injury. It also proposed a hypothetical scheme of how the disease develops.
• Who was studied: No new population was studied. The reviewed work was mainly on cultured human, rabbit and rat pleural mesothelial cells and on animal experiments, plus a limited number of clinical fibre burden studies.
• Exposure: Asbestos in the reviewed studies: amphiboles (crocidolite and amosite) and serpentine (chrysotile). These were compared in some studies with other particles such as alpha-cristobalite, alpha-quartz, carbonyl iron, polystyrene beads and riebeckite, a non-fibrous analogue of crocidolite.
• Main results:
  • Earlier fibre burden studies (Dodson et al. 1990; Gibbs et al. 1991), as described by the authors: all asbestos fibre types, long and short, can reach the visceral pleura. Only shorter chrysotile fibrils appeared to favour the parietal pleura and were found in pleural plaques and areas of diffuse pleural fibrosis.
  • Two cited studies (Boylan et al. 1992; Griffith et al. 1994b) reported that amosite, crocidolite and chrysotile increased interleukin-8 secretion by rabbit or human pleural mesothelial cells. The authors noted that a role for neutrophil recruitment in asbestos pleural injury has no clinical foundation, since benign asbestos effusions are comparatively rare.
  • A cited study (Kuwahara et al. 1994) found the following in rat pleural mesothelial cells. Crocidolite and chrysotile caused a dose-dependent release of fibronectin, which attracts lung fibroblasts, and uptake of the fibres by the cells was required. Carbonyl iron and alpha-quartz had no noticeable effect.
  • A cited study (Gelzleichter et al. 1994) reported increased collagen synthesis by rat pleural mesothelial cells after amosite exposure.
  • A cited study (Janssen et al. 1994) reported that crocidolite and chrysotile raised antioxidant gene expression in human pleural mesothelial cells, while polystyrene beads and riebeckite did not. Another cited study (Dong et al. 1994) suggested that oxygen radicals are only partly involved in asbestos effects on rat pleural mesothelial cells.
  • A cited study (Heintz et al. 1993) reported that crocidolite and chrysotile persistently activated the c-fos and c-jun genes in cultured rat pleural mesothelial cells, in a dose-dependent way. The authors suggested this may be one possible pathway toward diffuse malignant mesothelioma.
• The authors' conclusion: The authors suggested, as a hypothesis, the following sequence: the pleural mesothelial cell is the key effector cell, and the pleural macrophage is an important secondary participant, in asbestos-induced pleural fibrosis; the process starts when mesothelial cells take up asbestos fibres that have moved to the pleural space.
• Limitations the authors state:
  • Fibre burden evidence in humans came from only a limited number of clinical studies.
  • Evidence that mesothelial cells ingest asbestos fibres in living tissue came from animal experiments and had not been confirmed in human subjects.
  • To the authors' knowledge, no studies had examined the effect of asbestos on nitric oxide generation in mesothelial cells; the cited evidence came from rat alveolar macrophages.
  • The authors stated that existing theories of asbestos-induced pleural injury remained speculative, with very little factual evidence supporting them.

Topics

Medical terms in this study, explained in our Lexicon: Mesothelial Cells, Pleura, Fibrosis, Mesothelioma, Cytokine, Fibroblast, Chrysotile, Fibril.

Related studies

• Pleural macrophage recruitment and activation in asbestos-induced pleural injury — N. Choe, S. Tanaka, et al. (1997)
• beta1-integrin mediates asbestos-induced phosphorylation of AKT and ERK1/2 in a rat pleural mesothelial cell line — A. Berken, J. Abel, et al. (2003)
• Rat pleural mesothelial cells show damage after exposure to external but not internal cigarette smoke — H.S. Sekhon, B. Keeling, et al. (1993)
• Influence of metal ions on flavonoid protection against asbestos-induced cell injury — V.A. Kostyuk, A.I. Potapovich, et al. (2001)
• In vitro biodegradation of chrysotile fibres by alveolar macrophages and mesothelial cells in culture: comparison with a pH effect — M.C. Jaurand, A. Gaudichet, et al. (1984)
• Inflammatory Cytokines Contribute to Asbestos-Induced Injury of Mesothelial Cells — M.M. Acencio, B. Soares, et al. (2015)

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