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Editorial
. 2023 Nov 27;9(6):00647-2023.
doi: 10.1183/23120541.00647-2023. eCollection 2023 Nov.

A mechanistic insight into severe COPD: the nose as a surrogate for the airways

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Editorial

A mechanistic insight into severe COPD: the nose as a surrogate for the airways

Xin Yao et al. ERJ Open Res. .

Abstract

A severe COPD signature in bronchial and nasal epithelial cells reflects reduced tissue repair and ECM regulation https://bit.ly/476S3PJ.

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Conflict of interest statement

Conflict of interest: X. Yao and S. Mumby has nothing to disclose. I.M. Adcock reports investigator-led awards from GSK and Sanofi in addition to travel awards, speakers’ fees and advisory board fees from AZ, Chiesi, GSK, Eurodrug, Kineset, Sanofi and Sunovion outside the submitted work.

Figures

FIGURE 1
FIGURE 1
Overview of the study protocol. Bronchial brushings were obtained from patients with severe (n=123) and mild–moderate (n=23) COPD and 23 non-COPD control subjects and RNA sequencing performed. After identifying a set of differentially expressed genes between severe COPD and non-COPD subjects, genes within the dataset relating to mild–moderate COPD, specific cell subtypes and inhaled corticosteroid (ICS) use were removed to give a 219 gene severe COPD bronchial epithelial cell signature. Key down-regulated genes included fibronectin-1 (FN1) and vascular endothelial growth factor α (VEGFA) which were linked to suppression of extracellular matrix (ECM)- and tissue repair-associated pathways. The reduced expression of these genes and pathways were replicated in paired nasal bronchial brushings and in nasal epithelial cells from a separate cohort of severe COPD patients and non-COPD controls. mCOPD: moderate COPD.

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