Airway inflammation in COPD: progress to precision medicine.
Adrenal Cortex Hormones
/ therapeutic use
Biomarkers
/ metabolism
Eosinophils
/ metabolism
Humans
Inflammasomes
Inflammation
/ physiopathology
Neutrophils
/ metabolism
Phenotype
Precision Medicine
/ methods
Pulmonary Disease, Chronic Obstructive
/ physiopathology
Randomized Controlled Trials as Topic
Risk
Journal
The European respiratory journal
ISSN: 1399-3003
Titre abrégé: Eur Respir J
Pays: England
ID NLM: 8803460
Informations de publication
Date de publication:
08 2019
08 2019
Historique:
received:
31
03
2019
accepted:
25
04
2019
pubmed:
11
5
2019
medline:
30
9
2020
entrez:
11
5
2019
Statut:
epublish
Résumé
Chronic obstructive pulmonary disease (COPD) is a significant cause of morbidity and mortality worldwide, and its prevalence is increasing. Airway inflammation is a consistent feature of COPD and is implicated in the pathogenesis and progression of COPD, but anti-inflammatory therapy is not first-line treatment. The inflammation has many guises and phenotyping this heterogeneity has revealed different patterns. Neutrophil-associated COPD with activation of the inflammasome, T1 and T17 immunity is the most common phenotype with eosinophil-associated T2-mediated immunity in a minority and autoimmunity observed in more severe disease. Biomarkers have enabled targeted anti-inflammatory strategies and revealed that corticosteroids are most effective in those with evidence of eosinophilic inflammation, whereas, in contrast to severe asthma, response to anti-interleukin-5 biologicals in COPD has been disappointing, with smaller benefits for the same intensity of eosinophilic inflammation questioning its role in COPD. Biological therapies beyond T2-mediated inflammation have not demonstrated benefit and in some cases increased risk of infection, suggesting that neutrophilic inflammation and inflammasome activation might be largely driven by bacterial colonisation and dysbiosis. Herein we describe current and future biomarker approaches to assess inflammation in COPD and how this might reveal tractable approaches to precision medicine and unmask important host-environment interactions leading to airway inflammation.
Identifiants
pubmed: 31073084
pii: 13993003.00651-2019
doi: 10.1183/13993003.00651-2019
pii:
doi:
Substances chimiques
Adrenal Cortex Hormones
0
Biomarkers
0
Inflammasomes
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Department of Health
ID : PDF-2017-10-052
Pays : United Kingdom
Informations de copyright
Copyright ©ERS 2019.
Déclaration de conflit d'intérêts
Conflict of interest: C. Brightling reports grants and personal fees (paid to institution) for consultancy from MedImmune, AstraZeneca, GlaxoSmithKline, Roche/Genentech, Novartis, Chiesi, Pfizer and Mologic, personal fees (paid to institution) for consultancy from Teva, Sanofi, Regeneron, Glenmark and Vectura, outside the submitted work. Conflict of interest: N. Greening reports personal fees for consultancy and non-financial support for travel from AstraZeneca, Chiesi and Boehringer Ingelheim, grants, personal fees for consultancy and non-financial support for travel from GlaxoSmithKline, outside the submitted work.