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An airway epithelial IL-17A response signature identifies a steroid-unresponsive COPD patient subgroup
Journal article   Open access   Peer reviewed

An airway epithelial IL-17A response signature identifies a steroid-unresponsive COPD patient subgroup

Stephanie A Christenson, Maarten van den Berge, Alen Faiz, Kai Inkamp, Nirav Bhakta, Luke R Bonser, Lorna T Zlock, Igor Z Barjaktarevic, R Graham Barr, Eugene R Bleecker, …
The Journal of clinical investigation, Vol.129(1), pp.169-181
01/02/2019
DOI: 10.1172/JCI121087
PMCID: PMC6307967
PMID: 30383540
url
https://doi.org/10.1172/JCI121087View
Published (Version of record) Open Access

Abstract

Chronic obstructive pulmonary disease (COPD) is a heterogeneous smoking-related disease characterized by airway obstruction and inflammation. This inflammation may persist even after smoking cessation and responds variably to corticosteroids. Personalizing treatment to biologically similar "molecular phenotypes" may improve therapeutic efficacy in COPD. IL-17A is involved in neutrophilic inflammation and corticosteroid resistance, and thus may be particularly important in a COPD molecular phenotype. We generated a gene expression signature of IL-17A response in bronchial airway epithelial brushings from smokers with and without COPD (n = 238), and validated it using data from 2 randomized trials of IL-17 blockade in psoriasis. This IL-17 signature was related to clinical and pathologic characteristics in 2 additional human studies of COPD: (a) SPIROMICS (n = 47), which included former and current smokers with COPD, and (b) GLUCOLD (n = 79), in which COPD participants were randomized to placebo or corticosteroids. The IL-17 signature was associated with an inflammatory profile characteristic of an IL-17 response, including increased airway neutrophils and macrophages. In SPIROMICS the signature was associated with increased airway obstruction and functional small airways disease on quantitative chest CT. In GLUCOLD the signature was associated with decreased response to corticosteroids, irrespective of airway eosinophilic or type 2 inflammation. These data suggest that a gene signature of IL-17 airway epithelial response distinguishes a biologically, radiographically, and clinically distinct COPD subgroup that may benefit from personalized therapy. ClinicalTrials.gov NCT01969344. Primary support from the NIH, grants K23HL123778, K12HL11999, U19AI077439, DK072517, U01HL137880, K24HL137013 and R01HL121774 and contracts HHSN268200900013C, HHSN268200900014C, HHSN268200900015C, HHSN268200900016C, HHSN268200900017C, HHSN268200900018C, HHSN268200900019C and HHSN268200900020C.
Drug Resistance Adrenal Cortex Hormones - administration & dosage Aged Aged, 80 and over Bronchi - metabolism Bronchi - pathology Female Gene Expression Regulation - drug effects Humans Interleukin-17 - biosynthesis Male Middle Aged Psoriasis - drug therapy Psoriasis - metabolism Psoriasis - pathology Pulmonary Disease, Chronic Obstructive - drug therapy Pulmonary Disease, Chronic Obstructive - metabolism Pulmonary Disease, Chronic Obstructive - pathology

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