Asbestos-related increase in pulmonary levels of vasoactive intestinal peptide (VIP)

Our plain-English summary of Asbestos-related increase in pulmonary levels of vasoactive intestinal peptide (VIP), by R. Day, I. Lemaire, P. Mercier, et al (Life Sciences, 1983).

The study

• Authors: R. Day, I. Lemaire, P. Mercier, H. Beaudoin, S. Lemaire
• Journal: Life Sciences
• Published: 1983;33(19):1869-76
• Cited by: 16 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Vasoactive intestinal peptide (VIP), leucine-enkephalin (Leu-Enk), dynorphin (Dyn), neurotensin (NT) and substance P (SP) were measured by radioimmunoassay in lung and bronchoalveolar lavage (BAL) fluids of sham operated control rats and rats exposed to asbestos (5 and 10 mg, single intratracheal injections) for 3 and 6 months. Among these peptides, VIP, Leu-Enk and Dyn were the most abundant with 6 to 25 pmoles per g of lung tissue as compared with 0.95 to 1.2 pmoles per g for the other neuropeptides. In the presence of asbestos, VIP levels were selectively increased up to 2.7 times in lung tissue and 4.3 times in BAL fluids. On high pressure liquid chromatography (HPLC), the immunoreactive VIP coeluted with synthetic VIP. It is concluded that this selective increase may be involved in the pathogenesis of asbestos-related diseases. Exposure to asbestos causes chronic inflammatory reactions in the lung which may lead to fibrosis (1) and increase the incidence of pleuropulmonary cancers (2). Little is known concerning the biochemical changes responsible for the deleterious effects of asbestos on pulmonary functions. Previous studies have documented the vast complexity and diversity of lung biochemistry including its ability to metabolize lipids, inactivate certain enzymes and produce physiologically active amines (3-6). Recently, the lung has been recognized as an important source of peptidergic substances. VIP and SP were reported to be localized in nerve terminals of the main airways and in axons of the parasympathetic conducts (7-11). Other neuropeptides including bombesin (12, 13), calcitonin (13, 14) and Leu-Enk (13) were also detected in the lung. However, these latter peptides were mainly confined to diffuse granule-containing cells also known as APUD cells (amine precursor uptake and decarboxylation cells) (15). The role of these neuropeptides in normal lung function and in pulmonary diseases is unknown. However, it has recently been demonstrated that APUD cells proliferate in the rat lung following asbestos inhalation (16) and lung exposure to carcinogens (17, 18). In addition, Moody et al. (19) and Sorenson et al. (20) have observed high levels of bombesin in human cell lines derived from small-cell lung carcinoma. It was then of particular interest to verify if lung exposure to asbestos can induce some changes in the levels of various neuropeptides. In the present study, we report that VIP is significantly increased in the lungs and BAL fluids of rats exposed to asbestos while no significant change in the levels of Leu-Enk, Dyn, NT and SP is observed.

In plain English

This Sherbrooke, Quebec animal experiment gave three groups of 10 male Wistar rats one windpipe injection of saline (controls) or 5 or 10 mg of UICC Canadian Chrysotile B asbestos, killing them 3 and 6 months later. Five nerve-related peptides (VIP, leucine-enkephalin, dynorphin, neurotensin, substance P) were measured in lung tissue and lung-washing fluid, averaging 5 rats per value. Lung VIP was 6.0 pmoles per g in controls versus 11 (5 mg) and 12 (10 mg) at 3 months; at 6 months, 7.5 versus 19 and 20. Washing-fluid VIP rose from 1.2 to 4.0 pmoles per mg protein (10 mg) at 3 months, and from 1.0 to 3.7 (5 mg) and 4.3 (10 mg) at 6 months. VIP rises were statistically significant except the 5 mg 3-month washing-fluid value (2.0). The other four peptides showed no statistically significant change. At 3 months, treated lungs showed fibroblastic proliferation and collagen deposition (data not shown), with no evidence of pleuropulmonary tumors. The authors called the VIP rise's meaning uncertain, concluding it raises the question of VIP involvement in asbestos-related diseases' ongoing inflammation.

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 (rats given asbestos by single intratracheal injection, compared with saline-injected controls)
• Who was studied: Male Wistar rats weighing 200-235 g, in three groups of 10 (saline, 5 mg asbestos, 10 mg asbestos), killed at 3 and 6 months. Table values are means of 5 rats. The work was done at the Centre hospitalier universitaire de Sherbrooke, Quebec, Canada.
• Exposure: UICC Canadian Chrysotile B asbestos fibers, 5 mg or 10 mg in 0.25 ml saline, given once into the trachea; controls received saline
• Main results:
  • Lung tissue VIP at 6 months: 19 pmoles per g (5 mg group) and 20 pmoles per g (10 mg group), compared with 7.5 pmoles per g in controls (statistically different from controls, p less than 0.05)
  • Lung tissue VIP at 3 months rose 1.8-fold (5 mg group) and 2-fold (10 mg group), from 6 to 11 and 12 pmoles per g tissue
  • Lavage fluid VIP at 3 months in the 10 mg group: 4 pmoles per mg protein, compared with 1.2 pmoles per mg in controls
  • Lavage fluid VIP at 3 months in the 5 mg group was 2.0 pmoles per mg protein (167% of control). Table I does not mark this value as statistically different from controls.
  • Lavage fluid VIP at 6 months rose from 1.0 to 3.7 pmoles per mg protein in the 5 mg group (3.7 times control). In the 10 mg group it rose from 1.0 to 4.3 pmoles per mg (4.3-fold).
  • Lung levels of leucine-enkephalin, dynorphin, neurotensin and substance P showed no significant change in asbestos-exposed rats. The authors interpreted the effect as selective for VIP.
  • In lavage fluid, the only changes detected in response to asbestos involved VIP
  • At 3 months, lungs of treated rats showed fibroblastic proliferation and collagen deposition (data not shown)
  • The authors found no evidence of pleuropulmonary tumors in these animals
  • VIP in rat plasma was below 0.1 pmole per ml (data not shown). The authors judged the lung increase unlikely to come from blood.
• The authors' conclusion: The authors concluded that the study raises the question of a possible involvement of VIP in the continuing inflammatory processes found in asbestos-related diseases.
• Limitations the authors state:
  • The authors state that the disease meaning of the selective VIP increase in asbestos-exposed rat lungs is uncertain
  • The authors state it is not established whether the VIP changes are an early part of the lung reaction to asbestos or a consequence of the disease

Topics

Medical terms in this study, explained in our Lexicon: Bronchoalveolar Lavage (BAL), BAL Fluid, Fibrosis, Carcinoma.

Related studies

• Pulmonary bombesin in experimentally induced asbestosis in rats — R. Day, I. Lemaire, et al. (1985)
• Changes in autacoid and neuropeptide contents of lung cells in asbestos-induced pulmonary fibrosis — R. Day, S. Lemaire, et al. (1987)
• Alveolar macrophage stimulation of lung fibroblast growth in asbestos-induced pulmonary fibrosis — I. Lemaire, H. Beaudoin, et al. (1986)
• Asbestos-induced fibrosis in rats: increase in lung mast cells and autacoid contents — I. Keith, R. Day, et al. (1987)
• Cytokine regulation of lung fibroblast proliferation. Pulmonary and systemic changes in asbestos-induced pulmonary fibrosis — I. Lemaire, H. Beaudoin, et al. (1986)
• Exposure to low levels of ozone results in enhanced pulmonary retention of inhaled asbestos fibers — K.E. Pinkerton, A.R. Brody, et al. (1989)

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