Asbestos-induced release of a human alveolar macrophage-derived neutrophil chemotactic factor

Our plain-English summary of Asbestos-induced release of a human alveolar macrophage-derived neutrophil chemotactic factor, by A.A. Hayes, T.J. Venaille, A.H. Rose, et al (Experimental Lung Research, 1990).

The study

• Authors: A.A. Hayes, T.J. Venaille, A.H. Rose, A.W. Musk, B.W. Robinson
• Journal: Experimental Lung Research
• Published: 1990;16(2):121-30
• Cited by: 9 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Neutrophils accumulate in the alveoli of asbestos-exposed individuals. In determining whether asbestos fibers induce the release of neutrophil chemotactic factor (NCF) from human alveolar macrophages, alveolar macrophages (10(6) cell/mL) obtained by bronchoalveolar lavage from six non-asbestos-exposed control subjects were exposed to crocidolite (0.1 and 1 mg/mL), chrysotile (1 mg/mL), or medium alone for 4 h, and NCF activity was measured in the supernatants in a 48-well microchemotaxis chamber with polycarbonate membrane filters (pore size, 3 microns) and purified human neutrophils. Alveolar macrophages in medium alone released negligible amounts of NCF (4 +/- 1 neutrophils per high-power field [N/HPF]). When macrophages were exposed to crocidolite (0.1 and 1 mg/mL), significant NCF release occurred (43 +/- 9 and 105 +/- 32 N/HPF, respectively; p less than 0.01 for each amount compare to alveolar macrophages cultured in medium alone). Chrysotile (1 mg/mL) induced similar NCF release (96 +/- 14 N/HPF; p less than 0.01 compared to unstimulated alveolar macrophages). Partial characterization of the NCF by Sephadex G-25 fine gel filtration demonstrated a molecular size of less than 1,000 daltons. These results show that human alveolar macrophages release NCF after exposure to asbestos. Release of NCF by alveolar macrophages in asbestos-exposed individuals may play a central role in the pathogenesis of asbestosis.

In plain English

This laboratory study tested whether asbestos fibers directly cause human lung immune cells called alveolar macrophages to release neutrophil chemotactic factor (NCF), a substance that attracts neutrophils, a type of white blood cell. The macrophages were collected by lung washing (bronchoalveolar lavage) from six people with no history of asbestos exposure. In the lab, they were exposed to crocidolite (0.1 and 1 mg/mL), chrysotile (1 mg/mL), or medium alone. NCF activity was measured as the number of neutrophils that migrated per high-power microscope field, reported as an average plus or minus standard error. Macrophages in medium alone produced negligible NCF (4 ± 1). Crocidolite produced 43 ± 9 at 0.1 mg/mL and 105 ± 32 at 1 mg/mL, and chrysotile produced 96 ± 14. Each was statistically significant compared with medium alone (p less than 0.01). With either fiber, release was almost maximal at 2 hours. The factor was smaller than 1,000 daltons. The authors concluded that human alveolar macrophages release NCF after exposure to asbestos fibers. They also stated that its role in human asbestosis remains to be clarified.

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) experiment on human alveolar macrophages
• Who was studied: Alveolar macrophages obtained by bronchoalveolar lavage from six people with no history of asbestos exposure (five men, one woman; three smokers, three nonsmokers)
• Exposure: Reference samples of crocidolite at 0.1 and 1 mg/mL and intermediate-length chrysotile at 1 mg/mL, added to macrophages in culture; medium alone served as the comparison
• Main results:
  • Macrophages in medium alone produced negligible NCF: 4 ± 1 neutrophils per high-power field
  • Crocidolite at 0.1 mg/mL induced NCF release of 43 ± 9 neutrophils per high-power field (p less than 0.01 vs medium alone)
  • Crocidolite at 1 mg/mL induced NCF release of 105 ± 32 neutrophils per high-power field (p less than 0.01 vs medium alone)
  • Chrysotile at 1 mg/mL induced NCF release of 96 ± 14 neutrophils per high-power field (p less than 0.01 vs medium alone)
  • The positive-control stimulus, opsonized zymosan (0.1 mg/mL), induced NCF release of 105 ± 22 neutrophils per high-power field (p less than 0.01 vs medium alone)
  • With crocidolite or chrysotile, NCF release was almost maximal at 2 hours
  • By 8 and 24 hours, both fibers caused some cell damage: viability fell to 75 ± 21% and 49 ± 5% of control values, respectively
  • The asbestos-induced NCF had a molecular size of less than 1,000 daltons
• The authors' conclusion: The authors concluded that human alveolar macrophages release NCF after exposure to asbestos fibers
• Limitations the authors state:
  • The role of asbestos-induced NCF release in human asbestosis remains to be clarified
  • The NCF released after asbestos exposure has not been fully characterized

Topics

Medical terms in this study, explained in our Lexicon: Alveolar Macrophage, Alveoli, Bronchoalveolar Lavage (BAL), Crocidolite, Chrysotile, High-Power Field, Macrophage.

Related studies

• Neutrophil chemotactic factor release and neutrophil alveolitis in asbestos-exposed individuals — A.A. Hayes, A.H. Rose, et al. (1988)
• Pleural mesothelial cells stimulated by asbestos release chemotactic activity for neutrophils in vitro — V.B. Antony, C.L. Owen, 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)
• Time course of chemotactic factor generation and the corresponding macrophage response to asbestos inhalation — D.B. Warheit, L.H. Hill, 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)
• Distinctive profile of alveolar macrophage-derived cytokine release induced by fibrogenic and nonfibrogenic mineral dusts — I. Lemaire, S. Ouellet (1996)

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