Biochemical components of bronchoalveolar lavage in early experimental asbestosis of the sheep: phospholipase A2 activity, prostaglandin E2 and proteins

Our plain-English summary of Biochemical components of bronchoalveolar lavage in early experimental asbestosis of the sheep: phospholipase A2 activity, prostaglandin E2 and proteins, by P. Sirois, G. Drapeau, R. Bégin (Environmental Health Perspectives, 1983).

The study

• Authors: P. Sirois, G. Drapeau, R. Bégin
• Journal: Environmental Health Perspectives
• Published: 1983;51:293-8
• Cited by: 15 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Biochemical analyses of bronchoalveolar lavage (BAL) supernatants of sheep treated with weekly intratracheal instillations (for 6 months) of saline, 2 mg, or 128 mg of asbestos (chrysotile B; UICC) were performed. Our results showed that proteins (either total or its various components) and phospholipase A2 activity were unchanged in the low exposure group as compared to controls. However, in the high exposure group, with histopathological evidence of early asbestosis, there were significant increases in total proteins, albumin, alpha 2-globulin, beta- and gamma-globulins as well as phospholipase A2 activity of BAL fluid. Prostaglandin E2 activity was significantly increased in both low and high dose groups. These changes in protein and lipid components of BAL following asbestos exposure constitute early indices of lung inflammatory reactions which may contribute to the development of asbestosis.

In plain English

In this animal experiment, male sheep first received monthly doses of Canadian chrysotile B asbestos (UICC standard) into the windpipe: 1 to 16 mg for 3 months, then 2 to 128 mg for 3 months. The authors said the low-dose exposures produced no tissue or lung-function changes, so the treated sheep were regrouped into two groups of six, given 2 mg or 128 mg weekly. Controls received saline. The authors analyzed lung-washing fluid (bronchoalveolar lavage). In the 128 mg group, described as showing tissue evidence of early asbestosis, phospholipase A2 activity rose threefold, converting 3.23% of an added labeled phospholipid to fatty acids, against 1.16% in controls. Total protein, albumin, and beta and gamma globulins roughly doubled; alpha-2 globulin roughly tripled. Alpha-1 globulin did not change significantly. The 2 mg group did not differ from controls on these measures. Bioassayed prostaglandin E2-like activity was significantly higher in both dose groups. The authors concluded these changes are early signs of lung inflammation that may contribute to asbestosis. They said whether the changes cause or result from the inflammation remained open.

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: repeated intratracheal instillation of asbestos or saline in sheep, with monthly bronchoalveolar lavage and biochemical analysis of the lavage fluid; groups compared with Student's t-test
• Who was studied: Male sheep weighing 25-50 kg, at a research unit of the Université de Sherbrooke, Quebec, Canada. There were two asbestos-treated groups of six animals each. The number of control sheep is not stated in the readable text.
• Exposure: Canadian chrysotile B asbestos (UICC standard) in saline, instilled into the trachea. Sheep first received monthly doses of 1, 2, 4, 8 and 16 mg for 3 months, then doses between 2 and 128 mg for 3 more months. The authors stated that these low-dose exposures over 6 months failed to produce histopathological or functional changes. The sheep were then given weekly doses of either 2 mg or 128 mg for 6 months. Controls received weekly saline.
• Main results:
  • Phospholipase A2 activity was expressed as the percentage of added radiolabeled phosphatidylcholine converted to labeled fatty acids. In lavage fluid it was not changed in the 2 mg group (1.22%) compared with controls (1.16%).
  • In the 128 mg group, phospholipase A2 activity rose to 3.23% of the added labeled phosphatidylcholine converted to fatty acids. The authors report this threefold increase as significant.
  • Prostaglandin E2-like activity, measured by bioassay on rat stomach strips, was significantly increased in both the 2 mg and the 128 mg groups.
  • Prostaglandin E2-like activity averaged 0.26 ng/mL in controls, 0.5 ng/mL in the 2 mg group and 0.66 ng/mL in the 128 mg group. The authors said this suggested the inflammatory reactions were dose-dependent.
  • Total protein in lavage fluid was about 200 micrograms per mL in normal sheep. It was unchanged in the 2 mg group and more than doubled in the 128 mg group.
  • Albumin averaged about 100 micrograms per mL in controls and in the 2 mg group, and rose to about 200 micrograms per mL in the 128 mg group.
  • Alpha-2 globulin was about 10 micrograms per mL in the control and 2 mg groups, and rose significantly to about 30 micrograms per mL in the 128 mg group.
  • Beta and gamma globulins were about 100 micrograms per mL in the control and 2 mg groups, and rose significantly to about 200 micrograms per mL in the 128 mg group.
  • Alpha-1 globulins varied widely between animals and were not significantly changed by either dose.
  • Repeat measurements in the same sheep 1 and 2 months later gave very similar results.
• The authors' conclusion: The authors concluded that these protein and lipid changes in lavage fluid after asbestos exposure are early indices of lung inflammatory reactions that may contribute to the development of asbestosis, and could possibly serve as markers of early lung injury.
• Limitations the authors state:
  • The authors stated that their results cannot show whether the increased phospholipase A2 activity comes from activation of the enzyme, its production by lung cells, cell disruption by asbestos, or leakage from the blood.
  • The authors stated that it remains an open question whether the lipid and protein changes precede and cause the inflammatory reaction or result from it.

Topics

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

Medical terms in this study, explained in our Lexicon: Bronchoalveolar Lavage (BAL), Chrysotile, UICC, BAL Fluid, Asbestos Exposure.

Related studies

• Characterization of the bronchoalveolar cellular response in experimental asbestosis. Different reactions depending on the fibrogenic potential — I. Lemaire (1985)
• Assessment of progression of asbestosis in the sheep model by bronchoalveolar lavage and pulmonary function tests — R. Bégin, M. Rola-Pleszczynski, et al. (1983)
• The effects of chrysotile and crocidolite asbestos on the lower respiratory tract: analysis of bronchoalveolar lavage constituents — E. Kagan, Y. Oghiso, et al. (1983)
• Lymphocyte subpopulations in bronchoalveolar lavage fluid in asbestos workers — A.R. Gellert, M.G. Macey, et al. (1985)
• Fibronectin and procollagen 3 levels in bronchoalveolar lavage of asbestos-exposed human subjects and sheep — R. Bégin, M. Martel, et al. (1986)
• Morphologic features and function of the airways in early asbestosis in the sheep model — R. Bégin, S. Massé, et al. (1982)

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