ERS Respiratory Channel

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Abstract

Cigarette smoking is one of the most common causes of chronic obstructive pulmonary disease (COPD). In this study we aim to investigate the effect of cigarette smoke extract (CSE) on gene expression in lung fibroblasts from healthy and COPD subjects.

Lung fibroblasts from healthy and COPD subjects, mostly from smokers, were cultured and then stimulated with 0% or 30% CSE for 4 h. The mRNA expression was measured using the NanoString nCounter Human Fibrosis V2 panel. After pairwise comparison between 0% and 30% CSE, the functional annotations supplied by NanoString was used to compare the function of the genes with an altered expression.

Among the genes with a changed expression in response to CSE, 156 were altered in only healthy subjects, while 19 were altered in only COPD subjects. The functional annotations in the upregulated genes in the COPD subjects were related primarily to autophagy, programmed cell death, and endotoxin response, while fatty acid metabolism, collagen biosynthesis and modification, and neutrophil degranulation were the most common annotations in the healthy subjects. The functional annotations in the downregulated genes in the COPD subjects were primarily related to TGF-beta, the cell cycle, and autophagy, while epithelial to mesenchymal transitioning, MAPK cell stress, and the PI3K-akt pathway were the most common annotation in healthy subjects.

These results indicate a deficient response to CSE in COPD subjects and the function of the genes that had a change in expression in response to CSE did not overlap much between the healthy and COPD subjects. This could be a contributing factor to why some individuals develop COPD.

Abstract

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