Asbestos-induced alveolar injury. Evidence for macrophage-derived PDGF as a mediator of the fibrogenic response

Our plain-English summary of Asbestos-induced alveolar injury. Evidence for macrophage-derived PDGF as a mediator of the fibrogenic response, by J.C. Bonner, A.R. Brody (Chest, 1991).

The study

• Authors: J.C. Bonner, A.R. Brody
• Journal: Chest
• Published: 1991;99(3 Suppl):54S-55S
• Cited by: 14 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Summary of the article

The authors used asbestos exposure in rats and mice as a model of rapidly progressing interstitial lung fibrosis. They tested the idea that lung macrophages are the central mediators of the fibrogenic process, and focused on platelet-derived growth factor (PDGF), a growth factor for mesenchymal cells. In rats, alveolar macrophages were collected by lavage 1 week after a 3-hour inhalation exposure to chrysotile asbestos (10 mg/m3), carbonyl iron (50 mg/m3), a particle described as nonfibrogenic, or room air. Macrophages pooled from 3 to 4 rats were cultured in serum-free medium for 24 hours, and PDGF in the conditioned medium was measured by enzyme immunoassay. For comparison, macrophages from unexposed animals were exposed in culture to iron or asbestos for 24 hours. Results were the mean of 3 separate experiments. PDGF secretion by macrophages exposed by inhalation was 2.2- to 5.5-fold higher than after room air. In culture, iron and asbestos increased PDGF secretion 2.4- to 3.7-fold. Acid treatment of the medium was needed to detect most of the PDGF. The authors stated this was consistent with their earlier finding that much of this PDGF is bound to a macrophage-derived alpha-macroglobulin. They concluded that inhaled asbestos and iron increase PDGF secretion by lung macrophages. They proposed that asbestos may cause fibrosis by persisting in the lung and keeping macrophages activated over the long term.

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 short report described a laboratory study in rats. The authors tested whether lung immune cells called macrophages release a growth factor, platelet-derived growth factor (PDGF), that may drive lung scarring (fibrosis). Rats breathed chrysotile asbestos (10 mg/m3), carbonyl iron (50 mg/m3, described as a particle that does not cause fibrosis), or room air for 3 hours. One week later, macrophages were washed out of their lungs and grown in culture for 24 hours. In a parallel test, macrophages from unexposed rats were exposed to iron or asbestos directly in the culture dish. Macrophages from rats that breathed iron or asbestos released 2.2 to 5.5 times more PDGF than those from rats that breathed room air. In the dish, iron and asbestos raised PDGF release 2.4 to 3.7 times over untreated cells. The results came from 3 separate experiments. Most of the PDGF could be detected only after the culture fluid was acidified. The authors concluded that inhaling asbestos and iron increased PDGF release by lung macrophages. They proposed, as an idea still being tested, that asbestos may cause fibrosis by staying in the lung and keeping macrophages active over a long period.

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 (inhalation exposure of rats) with an in vitro comparison using cultured lung macrophages; brief conference-supplement report of ongoing studies
• Who was studied: Rats; alveolar macrophages pooled from 3 to 4 rats per culture; results from 3 separate experiments. Number of animals in total, location and dates not given.
• Exposure: Single 3-hour inhalation exposure to chrysotile asbestos (10 mg/m3), carbonyl iron (50 mg/m3, described as nonfibrogenic), or room air, with macrophages collected 1 week later. In vitro, macrophages from unexposed rats were exposed to suspensions of iron or asbestos for 24 hours.
• Main results:
  • Macrophages from rats exposed by inhalation to iron or asbestos secreted 2.2- to 5.5-fold more PDGF than macrophages from rats exposed to room air (range covers both particles)
  • Macrophages exposed in the culture dish to iron or asbestos secreted 2.4- to 3.7-fold more PDGF than macrophages attached to plastic only (range covers both particles)
  • Acidifying the macrophage culture fluid was necessary to detect most of the PDGF. The authors linked this to their earlier report that PDGF is bound to a macrophage-derived alpha-macroglobulin.
• The authors' conclusion: The authors concluded that inhaling asbestos and iron increased PDGF secretion by lung macrophages and that PDGF activity is modulated by alpha-macroglobulin. They postulated that asbestos may cause pulmonary fibrosis by persisting in the lung and causing long-term activation of lung macrophages. Whether PDGF is central to the progression of fibrosis was the subject of ongoing studies.

Topics

Medical terms in this study, explained in our Lexicon: Macrophage, Platelet-Derived Growth Factor (PDGF), Fibrogenic, Asbestos Exposure, Interstitial, Fibrosis, Alveolar Macrophage, Chrysotile.

Related studies

• Rat alveolar macrophage-derived platelet-derived growth factor is chemotactic for rat lung fibroblasts — A.R. Osornio-Vargas, J.C. Bonner, et al. (1990)
• Alveolar macrophage stimulation of lung fibroblast growth in asbestos-induced pulmonary fibrosis — I. Lemaire, H. Beaudoin, et al. (1986)
• Differential proliferation of rat lung fibroblasts induced by the platelet-derived growth factor-AA, -AB, and -BB isoforms secreted by rat alveolar macrophages — J.C. Bonner, A.R. Osornio-Vargas, et al. (1991)
• Rapid activation of PDGF-A and -B expression at sites of lung injury in asbestos-exposed rats — J.Y. Liu, G.F. Morris, et al. (1997)
• Secretion of fibronectin by mineral dust-derived alveolar macrophages and activated peritoneal macrophages — R. Davies, G. Erdogdu (1989)
• Inorganic particles induce secretion of a macrophage homologue of platelet-derived growth factor in a density-and time-dependent manner in vitro — R.M. Schapira, A.R. Osornio-Vargas, et al. (1991)

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