Pulmonary cell interactions with asbestos fibers in vivo and in vitro

Our plain-English summary of Pulmonary cell interactions with asbestos fibers in vivo and in vitro, by A.R. Brody (Chest, 1986).

The study

• Author: A.R. Brody
• Journal: Chest
• Published: 1986;89(3 Suppl):155S-159S
• Cited by: 14 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Summary of the article

This conference paper, presented at the 28th Annual Aspen Lung Conference, summarized studies from the author's laboratory at the National Institute of Environmental Health Sciences on how asbestos fibers interact with lung cells. It addressed four questions: where inhaled fibers land and how they move, which inflammatory cells respond, how the first lesion develops, and how fibers interact with cell membranes. In rats and mice that inhaled chrysotile or crocidolite for 1, 3 or 5 hours, scanning electron microscopy showed that most fibers were deposited at alveolar duct bifurcations. Shorter fibers were cleared earlier. One month after a 1-hour exposure, 20% of inhaled fibers remained, essentially all in the interstitium. Macrophages gathered at deposition sites within 48 hours. Complement-deficient mice and rats treated with cobra venom factor had significantly fewer macrophages there. Chemotactic activity was found in the 14-18,000-dalton range, which the author attributed most likely to C5a. Morphometry showed that macrophages and type I and II epithelial cells increased at bifurcations, with 10- to 25-fold increases in cells taking up tritiated thymidine. At one month, interstitial macrophages, fibroblasts and matrix were increased. In red blood cell and macrophage studies, positively charged chrysotile bound to sialic acid residues on cell membranes. The author concluded that the mechanisms remain largely undefined and that whether macrophage products cause disease in vivo remains to be determined.

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 1986 conference paper summarized research from the author's own laboratory, mostly already published elsewhere, on how asbestos fibers interact with lung cells in rats and mice and in cell experiments. It gave no animal numbers and only limited detail on methods. In animals that breathed chrysotile or crocidolite asbestos for 1, 3, or 5 hours, most fibers small enough to pass the airways landed first where alveolar ducts branch (bifurcations). After a 1-hour exposure, 20% of inhaled fibers remained one month later, essentially all within lung tissue (the interstitium). Macrophages, a type of immune cell, gathered at these sites within 48 hours of a 1-hour chrysotile exposure. Animals lacking part of the complement immune system had significantly fewer. One month later, interstitial macrophages, fibroblasts and collagen-rich tissue had increased. In red blood cell and macrophage experiments, chrysotile appeared to bind to sialic acid on cell surfaces. The author concluded that these interactions set off events leading to interstitial fibrosis. Whether macrophage products cause disease in living animals remained to be determined.

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: Conference paper summarizing the author's laboratory's animal inhalation experiments and in vitro cell studies (largely previously published work, cited by reference)
• Who was studied: Rats and mice exposed by inhalation (numbers not stated), plus red blood cells and pulmonary macrophages recovered by lavage from rat lungs, studied in vitro
• Exposure: Short-term inhalation of chrysotile or crocidolite asbestos for 1, 3, or 5 hours; in vitro exposure of red blood cells and macrophages to positively charged chrysotile and negatively charged crocidolite
• Main results:
  • In exposed rats and mice, most fibers small enough to pass the conducting airways were deposited initially at alveolar duct bifurcations
  • Shorter fibers were cleared earlier, leaving longer, thinner fibers in the lung interstitium; 20% of inhaled fibers were still in the lung 1 month after a 1-hour exposure
  • Pulmonary macrophages accumulated at alveolar duct bifurcations within 48 hours after a 1-hour chrysotile exposure
  • Complement-deficient animals (C5-deficient mice and rats treated with cobra venom factor) had significantly fewer macrophages at duct bifurcations after exposure than normal controls
  • In rats exposed for 1 hour, alveolar macrophages and type I and type II epithelial cells were significantly increased in number and volume at first alveolar duct bifurcations
  • In parallel autoradiography experiments, 10- to 25-fold increases in the numbers of cells incorporating tritiated thymidine were counted at bronchiolar-alveolar junctions
  • One month after a 1-hour exposure, interstitial macrophages and fibroblasts were increased and the noncellular interstitial matrix, mostly collagen, was increased in volume
  • 30 to 50% of first alveolar duct bifurcations contained intracellular microcalcifications, which the author described as a signal of membrane injury
  • Pretreating red blood cells with neuraminidase protected them from hemolysis by chrysotile but not by crocidolite
  • In rat macrophages, lectins that bind terminal sialic acid prevented binding and phagocytosis of positively charged particles but not negatively charged particles
• The authors' conclusion: The author concluded that interactions between inhaled fibers and lung cells induce a complex series of events resulting in interstitial fibrosis, but whether macrophage products play a disease-causing role in living animals remains to be determined
• Limitations the authors state:
  • Direct evidence that macrophage products cause interstitial disease is lacking
  • There are no data to explain the epithelial cell response

Topics

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

Medical terms in this study, explained in our Lexicon: Chrysotile, Crocidolite, Scanning Electron Microscopy (SEM), Macrophage, Deposition, Interstitial, Fibroblast.

Related studies

• Inhalable particles and pulmonary host defense: in vivo and in vitro effects of ambient air and combustion particles — G.E. Hatch, E. Boykin, et al. (1985)
• Phagocytosis of asbestos fibers by human pulmonary alveolar macrophages — T. McLemore, M. Corson, et al. (1979)
• In vitro interaction of zeolite fibers with individual cells (macrophages NR8383): measurement of intracellular oxidative burst — B.D. Hogg, P.K. Dutta, et al. (1996)
• Interaction of asbestos with alveolar cells — Y. Suzuki (1974)
• Chrysotile asbestos causes AEC apoptosis via the caspase activation in vitro and in vivo — T. Kido, Y. Morimoto, et al. (2008)
• Pulmonary macrophages are attracted to inhaled particles through complement activation — D.B. Warheit, L.H. Overby, et al. (1988)

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