Airways microbiota: Hidden Trojan horses in asbestos exposed individuals?

Our plain-English summary of Airways microbiota: Hidden Trojan horses in asbestos exposed individuals?, by D.E. Magouliotis, V.S. Tasiopoulou, P.A. Molyvdas, et al (Medical Hypotheses, 2014).

The study

• Authors: D.E. Magouliotis, V.S. Tasiopoulou, P.A. Molyvdas, K.I. Gourgoulianis, C. Hatzoglou, S.G. Zarogiannis
• Journal: Medical Hypotheses
• Published: 2014;83(5):537-40
• Cited by: 3 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Malignant pleura mesothelioma (MPM) is a rare type of cancer with devastating prognosis, which develops in the pleural cavity from transformed mesothelium. MPM has been directly associated with asbestos exposure however there are aspects of the pathophysiology involved in the translocation of asbestos fibers in the pleura that remain unclear. Here, we propose and discuss that certain proteins secreted by airways symbiotic microbiota create membrane pores to the airway epithelial cells, through which asbestos fibers can penetrate the lung parenchyma and reach the sub-pleural areas. We evaluate this hypothesis using data from the published literature regarding the airways microbiota toxins such as cholesterol-dependent cytolysins (CDCs).

Copyright © 2014 Elsevier Ltd. All rights reserved.

In plain English

This article proposed an idea. It reported no new data from patients, workers or experiments. The authors asked how inhaled asbestos fibers might reach the pleura, where malignant pleural mesothelioma develops. They hypothesized that proteins released by bacteria that normally live in the airways create pores in airway cells, and that very thin asbestos fibers could pass through those pores. To evaluate this, they searched published literature for pore-forming toxins made by the three most common airway bacterial families reported in an earlier study. Their literature search found no toxins meeting their criteria in Veillonellaceae or Prevotellaceae. In the Streptococcaceae family they identified five toxins of a type called cholesterol-dependent cytolysins (PLY, SLO, ILY, MLY and LLY), made by Streptococcus pneumoniae, S. pyogenes, S. intermedius and S. mitis. The authors described these toxins as forming pores wider than the thinnest asbestos fibers. The authors stated that their hypothesis had yet to be tested and proposed a simple laboratory experiment to test it. The article did not name specific asbestos fiber types.

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: Hypothesis article evaluated using published literature; no original data
• Who was studied: No people were studied. The authors reviewed literature on the three most prevalent bacterial families of the airway flora, as identified in an earlier study by Charlson et al.
• Exposure: Inhaled asbestos fibers in general, with a focus on ultrathin fibers about 20 to 200 nm wide (based on other studies); no fiber type was named
• Main results:
  • From their literature search, the authors reported that cholesterol-dependent cytolysins (CDCs) were the only family of pore-forming toxins producing pores of the size needed for ultrathin fibers to pass
  • The literature search found no agents meeting the hypothesis criteria in the most prevalent airway family, Firmicutes Veillonellaceae
  • The literature search found no results meeting the hypothesis criteria in the second most prevalent family, Bacteroidetes Prevotellaceae
  • Five CDC toxins (PLY, SLO, ILY, MLY and LLY), produced by Streptococcaceae species (S. pneumoniae, S. pyogenes, S. intermedius and S. mitis), were identified as possibly fitting the proposed mechanism
  • The authors described these toxins as producing pores wider than the thinnest asbestos fibers
  • The pneumolysin (PLY) pore was described as having a mean diameter of 25 nm
• The authors' conclusion: The authors concluded that certain CDC toxins from bacteria of the natural respiratory flora seem to fit their proposed mechanism of asbestos fiber translocation to the pleural cavity
• Limitations the authors state:
  • The hypothesis has not been tested in practice; the authors proposed a simple experimental strategy to test it

Topics

The National Library of Medicine indexes this study under subjects our site covers: Lung cancer, Mesothelioma.

Medical terms in this study, explained in our Lexicon: Pleura, Mesothelioma, Prognosis, Pleural Cavity, Mesothelium, Asbestos Exposure, Translocation, Parenchyma.

Related studies

• Effects of cigarette smoke and asbestos on airway, vascular and mesothelial cell proliferation — H. Sekhon, J. Wright, et al. (1995)
• Irregular opacities in the lung, occupational asthma, and airways dysfunction in aluminum workers — K.H. Kilburn, R.H. Warshaw (1992)
• Inhalation and Oropharyngeal Aspiration Exposure to Rod-Like Carbon Nanotubes Induce Similar Airway Inflammation and Biological Responses in Mouse Lungs — P. Kinaret, M. Ilves, et al. (2017)
• Airway function in lifetime-nonsmoking older asbestos workers — R. Bégin, A. Cantin, et al. (1983)
• Morphologic features and function of the airways in early asbestosis in the sheep model — R. Bégin, S. Massé, et al. (1982)
• Asbestos fiber content of the lungs in patients with and without asbestos airways disease — A. Churg (1983)

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