Pulmonary bombesin in experimentally induced asbestosis in rats

Our plain-English summary of Pulmonary bombesin in experimentally induced asbestosis in rats, by R. Day, I. Lemaire, S. Masse, et al (Experimental Lung Research, 1985).

The study

• Authors: R. Day, I. Lemaire, S. Masse, S. Lemaire
• Journal: Experimental Lung Research
• Published: 1985;8(1):1-13
• Cited by: 24 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

The pulmonary levels of immunoreactive bombesin in normal rat lungs and rat lungs exposed to asbestos were determined. Experimental asbestosis was induced in rats by a single intratracheal injection of 5 mg or 10 mg UICC standard Canadian Chrysotile B while sham-operated control rats received only the saline carrier. At 1, 3, 6, and 9 months following instillation, 5 animals of each group were sacrificed and the lungs removed. A section was kept for morphologic analysis, while the remaining portion was submitted to acid extraction and later measured for bombesin content by radioimmunoassay (RIA). The Chrysotile B-exposed tissues displayed the characteristic features typical of the fibrotic state associated with asbestosis one month following exposure and thereafter. The pulmonary bombesinlike immunoreactivity ranged from 4.5-7.5 pmoles/g tissue in normal rat lung, and these levels remained unchanged at 1 and 3 months after asbestos exposure. However at 6 and 9 months, significant increases ranging between 2 and 2.5 fold were observed. The initial increases in bombesin levels occurred at a later time (6 months) than those already observed for vasoactive intestinal peptide (VIP) (3 months). However, VIP levels plateaued at 9 months, while those of bombesin were still increasing. High-pressure liquid chromatography (HPLC) coupled with RIA demonstrates the presence of two bombesin-immunoreactive peaks in normal rat lung, the major one coeluting with the mammalian bombesinlike peptide gastrin-releasing peptide (GRP) and the other one being presumably a C-terminal portion of GRP. These data indicate that immunoreactive bombesin and VIP are selectively increased at different times following asbestos instillation and that these changes occur after the onset of fibrosis and the appearance of well-defined fibrotic lesions.

In plain English

This animal experiment used male Wistar rats. Three groups of 20 rats received one injection into the windpipe of saline (controls) or 5 mg or 10 mg of UICC Canadian Chrysotile B asbestos. Lungs were examined 1, 3, 6 and 9 months later. All animals survived. Exposed lungs weighed 30-55% more than control lungs and showed fibrosis around small airways from one month. No lung or pleural tumors were found. The researchers measured bombesin-like immunoreactivity, which in normal lung came mainly from gastrin-releasing peptide (GRP); normal lungs had 4.5-7.5 pmoles/g. In exposed lungs this did not change significantly at 1 and 3 months but rose significantly at 6 and 9 months. At 9 months it went from 7.5 to 15 pmoles/g (5 mg dose) and 19 pmoles/g (10 mg dose); which form rose was not determined. VIP, a peptide the authors had studied earlier, rose from 3 months. The authors concluded that these changes came after the fibrosis, suggesting the peptides may be involved in later disease stages. They noted the method spread fibers unevenly in the lung.

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 (asbestos instilled directly into the trachea of rats, with saline-treated controls)
• Who was studied: Male Wistar rats from Charles River Canada, in three groups of 20 rats each (saline controls, 5 mg asbestos, 10 mg asbestos), examined at 1, 3, 6 and 9 months. Five extracts per group and time point were measured. The study dates are not given.
• Exposure: A single intratracheal injection of 5 mg or 10 mg UICC standard Canadian Chrysotile B asbestos. Sham-operated controls received only the saline carrier.
• Main results:
  • There was no difference in survival between saline-treated and asbestos-treated rats. All animals survived.
  • Lungs of asbestos-exposed rats weighed 30-55% more than control lungs (p less than .05). The difference appeared at one month and persisted throughout the experiment.
  • Asbestos-exposed lungs showed peribronchiolitis and bronchiolitis obliterans (fibroblast proliferation and collagen around small airways) at 1 month and at 3, 6 and 9 months. No pleuropulmonary tumors were found.
  • In normal rat lung, immunoreactive bombesin (bombesin-like immunoreactivity) ranged from 4.5 to 7.5 pmoles/g of tissue.
  • In exposed lungs, bombesin immunoreactive content showed no significant change at 1 and 3 months but increased significantly at 6 and 9 months, with both the 5 mg and 10 mg doses.
  • The article reports 2.1-fold (5 mg) and 2.4-fold (10 mg) increases in immunoreactive bombesin, from 4.5 to 9.5 and 11 pmoles/g tissue. By context this refers to 6 months, though the sentence does not name the time point.
  • At 9 months, immunoreactive bombesin rose 2-fold (5 mg) and 2.5-fold (10 mg), from 7.5 to 15 and 19 pmoles/g tissue respectively.
  • VIP levels, plotted alongside and drawing on the authors' earlier report, were unchanged at 1 month. They rose significantly from 3 months and plateaued at 9 months (1.8- to 2.6-fold increases).
  • Because exposed lungs were heavier, the authors estimated that the changes in VIP and bombesin per whole lung were four to five times normal levels.
  • Chromatography of normal rat lung extract showed two bombesin-immunoreactive forms. The major one corresponded to gastrin-releasing peptide (GRP), and the minor one was most probably a C-terminal fragment of GRP.
• The authors' conclusion: The authors concluded that the increases in VIP and bombesin immunoreactivities came after the fibrotic lesions characteristic of asbestosis, suggesting that VIP and a bombesin-like peptide (GRP) may be involved in the later stages of the condition.
• Limitations the authors state:
  • The method used to induce experimental asbestosis did not distribute the asbestos fibers uniformly in the lung.
  • The rat model greatly speeds up the development and effects of asbestosis compared with the human disease.
  • The authors did not know whether one or both of the bombesin-immunoreactive forms accounted for the increase. The reported levels are the sum of both peaks.

Topics

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

Medical terms in this study, explained in our Lexicon: UICC, Chrysotile, Asbestos Exposure, Fibrosis.

Related studies

• The release of bombesin-like peptides from small cell lung cancer cells — T.W. Moody, L.Y. Korman (1988)
• Changes in autacoid and neuropeptide contents of lung cells in asbestos-induced pulmonary fibrosis — R. Day, S. Lemaire, et al. (1987)
• Chrysotile-induced asbestosis: changes in the free cell population, pulmonary surfactant and whole lung tissue of rats — T.D. Tetley, P.M. Hext, et al. (1976)
• Asbestos-induced fibrosis in rats: increase in lung mast cells and autacoid contents — I. Keith, R. Day, et al. (1987)
• Experimentally induced mesothelioma in white rats in response to intraperitoneal administration of amorphous crocidolite asbestos: preliminary report — K. Kolev (1982)
• Asbestos-related increase in pulmonary levels of vasoactive intestinal peptide (VIP) — R. Day, I. Lemaire, et al. (1983)

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