Abstract

YKL-40 is a chitinase-like glycoprotein produced by alternatively activated macrophages that are associated with wound healing and fibrosis. Asbestosis is a chronic asbestos-induced lung disease, in which injury of epithelial cells and activation of alveolar macrophages lead to enhanced collagen production and fibrosis. We studied if YKL-40 is related to inflammation, fibrosis, and/or lung function in subjects exposed to asbestosis. Venous blood samples were collected from 85 men with moderate or heavy occupational asbestos exposure and from 28 healthy, age-matched controls. Levels of plasma YKL-40, CRP, IL-6, adipsin, and MMP-9 were measured with enzyme-linked immunosorbent assay (ELISA). Plasma YKL-40 levels were significantly higher in subjects with asbestosis (n = 19) than in those with no fibrotic findings in HRCT following asbestos exposure (n = 66) or in unexposed healthy controls. In asbestos-exposed subjects, plasma YKL-40 correlated negatively with lung function capacity parameters FVC (Pearson's r −0.259, p = 0.018) and FEV1 (Pearson's r −0.240, p = 0.028) and positively with CRP (Spearman's rho 0.371, p < 0.001), IL-6 (Spearman's rho 0.314, p = 0.003), adipsin (Spearman's rho 0.459, p < 0.001), and MMP-9 (Spearman's rho 0.243, p = 0.025). The present finding suggests YKL-40 as a biomarker associated with fibrosis and inflammation in asbestos-exposed subjects.

Highlights

  • Asbestosis is a chronic interstitial fibrosing lung disease developing slowly after exposure to asbestos fibers

  • YKL-40 is a chitinase-like glycoprotein produced by alternatively activated macrophages that are associated with wound healing and fibrosis

  • We studied if YKL-40 is related to inflammation, fibrosis, and/or lung function in subjects exposed to asbestosis

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Summary

Introduction

Asbestosis is a chronic interstitial fibrosing lung disease developing slowly after exposure to asbestos fibers. As the clearance of these fibers is very slow, exposure to asbestos can lead to chronic inflammatory changes and eventually to clinically detectable fibrosis after a latent period. As fibrosis manifests 15 to 40 years after exposure to asbestos and highest level of asbestos use took place in the 1970s and 1980s in European countries, peak in the incidence of asbestos-related diseases is levelling off [1, 4]. Investigation of inflammatory and fibrotic processes in asbestosis is needed to allow drug development and to find novel biomarkers to diagnose and follow up these diseases [6]

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