Asbestos stimulates alveolar macrophages to release a factor causing human lung fibroblasts to replicate

Our plain-English summary of Asbestos stimulates alveolar macrophages to release a factor causing human lung fibroblasts to replicate, by P. Bitterman, S. Rennard, C. Schoenberger, et al (Chest, 1981).

The study

• Authors: P. Bitterman, S. Rennard, C. Schoenberger, R. Crystal
• Journal: Chest
• Published: 1981;80(1 Suppl):38-9
• Cited by: 9 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Summary of the article

This short report, published in a conference supplement, asked whether pulmonary alveolar macrophages (PAM) help form the clusters of lung fibroblasts seen around macrophages that have engulfed asbestos fibers in asbestosis. The authors tested whether PAM release soluble factors that make human lung fibroblasts replicate. PAM taken from minced guinea pig lung were incubated for four hours in culture medium with 0.5% fetal calf serum, with or without 100 µg/ml short chrysotile asbestos (fibers under 5 µm long). The supernatants, free of asbestos fibers, were placed on steady-state human lung fibroblasts. Cell counts were taken after one, two and four days. Medium with or without asbestos, incubated without macrophages, served as controls. Supernatants from unexposed PAM did not change the fibroblast replication rate. Supernatants from asbestos-exposed PAM significantly increased replication: doubling time fell about five-fold, from 310±21 hours in controls to 54±4 hours (P<.001). By 48 hours, treated plates had 68±2 cell-count units per plate against 43±3 in controls. The authors concluded that asbestos-treated PAM release a factor or factors that promote human lung fibroblast replication. They suggested PAM may have a role in forming the fibroblast clusters seen in early asbestosis. In the discussion, Dr. Bitterman said the effect was most likely not specific to asbestos. He reported that asbestos and medium without macrophages produced no growth factor, and that the factor was heat stable and was also obtained without serum.

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 was a short laboratory report in conference proceedings, with a recorded discussion. It looked at whether alveolar macrophages (scavenger cells from the lung) release a substance that makes human lung fibroblasts multiply. Fibroblast clusters around macrophages that have swallowed fibers are a typical finding in asbestosis. The macrophages came from guinea pig lung. They were incubated for four hours with or without short chrysotile asbestos (fibers shorter than 5 micrometres). The fluid from these cells, free of fibers, was then put on human lung fibroblasts. Fluid from macrophages not exposed to asbestos did not change how fast the fibroblasts multiplied. Fluid from asbestos-exposed macrophages significantly sped up fibroblast multiplication, cutting the doubling time five-fold from 310 plus or minus 21 hours to 54 plus or minus 4 hours. In the discussion, the presenting author said asbestos and medium alone, without macrophages, produced no growth factor. The authors concluded that this suggests a possible role for these macrophages in forming the fibroblast clusters of early asbestosis. The presenting author also said the effect was most likely not specific to asbestos, which alone had been tested.

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: Laboratory (in vitro) cell-culture experiment, published as a short conference report with discussion
• Who was studied: Pulmonary alveolar macrophages from minced guinea pig lung, and cultured human lung fibroblasts; numbers of cultures not stated
• Exposure: Short chrysotile asbestos (printed 'crysotile'), 100 micrograms per ml, fiber length less than 5 micrometres, incubated with the macrophages for four hours
• Main results:
  • Fluid from macrophages not exposed to asbestos had no influence on the rate at which fibroblasts multiplied
  • Fluid from asbestos-exposed macrophages significantly increased the rate of fibroblast doubling, shortening doubling time five-fold from a control of 310 plus or minus 21 hours to 54 plus or minus 4 hours. The P value is garbled in the scan (printed as 'P<.OOI').
  • At 48 hours, plates treated with fluid from asbestos-exposed macrophages had 68 plus or minus 2 cell-count units per plate, compared with 43 plus or minus 3 in the control groups. The power-of-ten multiplier is garbled in the scan.
  • Incubating fibroblasts with medium and asbestos but no macrophages produced no growth factor (stated in the discussion)
  • The presenting author reported that the factor was also obtained without serum and that it is heat stable (stated in the discussion)
• The authors' conclusion: The authors concluded that asbestos-treated macrophages release a factor or factors that promote human lung fibroblast replication. They wrote that this suggests a possible role for these macrophages in forming the fibroblast clusters seen in early asbestosis.
• Limitations the authors state:
  • The presenting author said the effect is most likely not specific for asbestos, and it is not known whether growth factors released after other stimuli are identical
  • Only asbestos was tested; no comparison substance such as beryllium was used

Topics

Medical terms in this study, explained in our Lexicon: Alveolar Macrophage, Fibroblast, Macrophage, Chrysotile.

Related studies

• Asbestos fibers and silica particles stimulate rat alveolar macrophages to release tumor necrosis factor. Autoregulatory role of leukotriene B4 — C.M. Dubois, E. Bissonnette, et al. (1989)
• 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)
• Asbestos-stimulated tumour necrosis factor release from alveolar macrophages depends on fibre length and opsonization — K. Donaldson, X.Y. Li, et al. (1992)
• Alveolar macrophages from patients with asbestos exposure release increased levels of leukotriene B4 — J.G. Garcia, D.E. Griffith, et al. (1989)
• Effects of asbestos and beryllium on release of alveolar macrophage enzymes — K.Y. Kang, D. Bice, et al. (1979)

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