Fibrogenic effects of crocidolite, amosite, and chrysotile asbestos fibers on lung fibroblasts

Abstract

Asbestos causes fibrotic lung diseases such as asbestosis and lung scarring, but the molecular mechanisms underlying the effects of specific types of asbestos fibers are not fully understood. The objective of this study was to investigate the fibrogenic activity of commonly used asbestos types crocidolite (serpentine) and amosite and chrysotile (amphiboles) which differ in general toxicity. IMR-90 lung fibroblasts were exposed to various concentrations of crocidolite, amosite, and chrysotile and analyzed for viability, adhesion, cell damage, functional activity, and expression of genes associated with fibrosis, cell stress, and toxicity responses. Exposure of fibroblasts to the three asbestos fibers for 48 h did not affect cellular functions such as filamentous actin distribution and mitochondrial activity. PCR microarray profiling of the expression of 84 genes central to fibrogenesis revealed that chrysotile significantly upregulated the transcription of genes encoding pro-fibrotic cytokines and downregulated genes related to the transforming growth factor-beta superfamily, whereas the effects of crocidolite and amosite on pro-fibrotic gene expression were much weaker. There was no significant difference in the expression of oxidative stress- and toxic response-related genes among the three asbestos types. These results provide new evidence that chrysotile has a stronger pro-fibrotic potential than amosite and crocidolite.

Keywords:

• Chrysotile
• amosite
• crocidolite
• lung fibrosis
• fibroblast
• oxidative stress

Acknowledgments

We would like to thank Jeffrey D. Rimer for his helpful comments on this work.

Data availability statement

The authors confirm that the data supporting the findings of this study are available within the article and its supplementary materials.

Geolocation information

South Korea

Disclosure statement

No potential conflict of interest is reported by the authors.

Additional information

Funding

This work was supported by the National Research Foundation of Korea (NRF) funded by the Korea government (MSIT) under Grant number [2017R1E1A1A01078335], the Catholic Medical Center Research Foundation (program year 2019), and the Institute of Clinical Medicine Research, Yeouido St. Mary’s Hospital.