Adipokine adipsin is associated with the degree of lung fibrosis in asbestos-exposed workers

Our plain-English summary of Adipokine adipsin is associated with the degree of lung fibrosis in asbestos-exposed workers, by S. Leivo-Korpela, L. Lehtimäki, R. Nieminen, et al (Respiratory Medicine, 2012).

The study

• Authors: S. Leivo-Korpela, L. Lehtimäki, R. Nieminen, P. Oksa, T. Vierikko, R. Järvenpää, J. Uitti, E. Moilanen
• Journal: Respiratory Medicine
• Published: 2012;106(10):1435-40
• Cited by: 12 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Objectives: Asbestos-exposure causes an inflammatory response driven by alveolar macrophages that can lead to pulmonary fibrosis. In addition to classical inflammatory cytokines, macrophages produce adipokines which regulate the inflammatory response. We studied if adipokines are related to the degree of parenchymal fibrosis, impaired lung function and inflammation in asbestos-exposed subjects.

Methods: Eighty-five males with moderate to heavy occupational exposure to asbestos and unexposed controls were studied. We measured plasma levels of adipokines adiponectin, adipsin, leptin and resistin, IL-6, IL-8, erythrocyte sedimentation rate (ERS), spirometry and D(L,CO). Degree of interstitial lung fibrosis (septal thickening, subpleural lines, parenchymal bands or honeycombing) was scored in classes 0-5 according to a validated scoring system. The subjects were divided into three groups: normal parenchymal finding (fibrosis class 0), borderline changes (classes 0.5-1.5) and fibrosis (i.e. asbestosis; classes 2-5).

Results: Adipsin correlated positively with parenchymal fibrosis (rho=0.412, p<0.001) and there was a linear increasing trend of mean plasma adipsin levels among the three groups of asbestos-exposed subjects (from normal parenchymal finding to borderline changes and to fibrosis) (p<0.0001). Accordingly, plasma adipsin levels correlated positively with the extent of pleural plaques (r=0.245, p=0.043), and negatively with D(L,CO) (r=-0.246, p=0.023). Also, a positive correlation was found between adipsin and inflammatory markers ESR (r=0.315, p=0.008) and IL-6 (r=0.256, p=0.018).

Conclusions: Adipsin was associated with the degree of parenchymal fibrosis, impairment of pulmonary diffusing capacity and with inflammatory activity in asbestos-exposed subjects suggesting that adipsin may have a role in the pathogenesis or as a biomarker in asbestos-induced lung disease.

Copyright © 2012 Elsevier Ltd. All rights reserved.

In plain English

This Finnish study examined whether blood levels of adipokines, proteins that help regulate inflammation, were linked to lung scarring in men occupationally exposed to asbestos. Of 118 men with moderate or heavy exposure recruited at Tampere University Hospital, 33 were excluded for other lung conditions, leaving 85. Twenty-eight unexposed healthy men served as controls. On lung CT scans, 35 exposed men had normal lung tissue (parenchyma), 31 had borderline changes and 19 had fibrosis regarded as asbestosis. Of the four adipokines measured, only adipsin was linked to fibrosis grade (Spearman's rho 0.412, p less than 0.001), and its levels rose from normal to borderline to fibrosis. Adipsin was higher in men with fibrosis than in exposed men without fibrosis and than in controls. Among exposed men, higher adipsin went with more pleural plaques, poorer diffusing capacity, and higher levels of the inflammation markers ESR and IL-6. The authors concluded that adipsin may have a role in asbestos-induced lung disease or serve as a biomarker. They noted that it might merely mark macrophage activation and that it was unclear whether the link is specific to asbestos.

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: Cross-sectional comparison: asbestos-exposed men grouped by CT (HRCT) findings and compared with unexposed controls, with correlation analyses
• Who was studied: 118 men with moderate or heavy occupational asbestos exposure recruited at the Clinic of Occupational Medicine, Tampere University Hospital, Finland. 33 were excluded (16 for FEV1/FVC below 0.70, 11 for emphysema or bronchiectasis on HRCT, 6 for asthma or asthma medication), leaving 85: 35 with normal parenchymal findings, 31 with borderline parenchymal changes and 19 with pulmonary fibrosis regarded as asbestosis. Pleural plaques were scored separately from parenchymal fibrosis. 28 healthy unexposed men were controls. All subjects were never smokers or had quit at least 5 years earlier. Study dates were not given.
• Exposure: Moderate or heavy occupational exposure to asbestos, estimated at at least 20 fibre years. Fiber types and jobs were not specified.
• Main results:
  • Among exposed men, adipsin (but no other adipokine) correlated positively with HRCT fibrosis class 0 to 5: Spearman's rho 0.412, p less than 0.001
  • There was a statistically significant (p less than 0.0001) increasing linear trend in adipsin across the three exposed groups, from normal to borderline to fibrosis on HRCT
  • Adipsin was higher in exposed men with pulmonary fibrosis than in exposed men with no parenchymal fibrosis (p = 0.013) or unexposed controls (p = 0.038). Mean adipsin (ng/ml) was 871 in no fibrosis, 965 in borderline, 1129 in fibrotic and 906 in controls.
  • In the 85 exposed men, adipsin correlated positively with extent of pleural plaques (r = 0.245, p = 0.043) and negatively with diffusing capacity DL,CO (r = -0.246, p = 0.023)
  • In exposed men, adipsin correlated with ESR (r = 0.315, p = 0.008) and plasma IL-6 (r = 0.256, p = 0.018)
  • There were no significant group differences in adiponectin, leptin or resistin. Resistin correlated positively with IL-6, but adiponectin and leptin did not correlate significantly with lung function, plaques or inflammatory markers.
• The authors' conclusion: The authors concluded that adipsin may have a role in the pathogenesis of asbestos-induced lung injury or serve as a biomarker, and that further studies are needed to see if it could be used as a prognostic tool.
• Limitations the authors state:
  • Adipsin could be merely a marker of alveolar macrophage activation rather than a cause; further studies are needed
  • It is not clear whether adipsin is specifically associated with asbestos or also with other fibrosing lung diseases
  • Further studies are needed on whether other interstitial lung diseases or current smoking could affect adipsin levels

Topics

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

Medical terms in this study, explained in our Lexicon: Fibrosis, Alveolar Macrophage, Pulmonary Fibrosis, Cytokine, Macrophage, Interstitial Fibrosis, Inflammation, Occupational Exposure.

Related studies

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• Comparative quantitative evaluation of pleural fibrosis and its effects on pulmonary function in two large asbestos-exposed occupational groups--insulators and sheet metal workers — R. Lilis, A. Miller, et al. (1992)
• Glycoprotein YKL-40 Levels in Plasma Are Associated with Fibrotic Changes on HRCT in Asbestos-Exposed Subjects — T. Väänänen, L. Lehtimäki, et al. (2017)
• Relation of spirometric function to radiographic interstitial fibrosis in two large workforces exposed to asbestos: an evaluation of the ILO profusion score — A. Miller, R. Lilis, et al. (1996)
• Asbestos-related pleural and lung fibrosis in patients with retroperitoneal fibrosis — T. Uibu, R. Järvenpää, et al. (2008)
• Parenchymal and pleural fibrosis in construction workers — P. Oksa, H. Koskinen, et al. (1992)

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