How inhaled corticosteroids target inflammation in COPD.


Journal

European respiratory review : an official journal of the European Respiratory Society
ISSN: 1600-0617
Titre abrégé: Eur Respir Rev
Pays: England
ID NLM: 9111391

Informations de publication

Date de publication:
31 Dec 2023
Historique:
received: 24 04 2023
accepted: 05 06 2023
medline: 23 10 2023
pubmed: 19 10 2023
entrez: 18 10 2023
Statut: epublish

Résumé

Inhaled corticosteroids (ICS) are the most commonly used anti-inflammatory drugs for the treatment of COPD. COPD has been previously described as a "corticosteroid-resistant" condition, but current clinical trial evidence shows that selected COPD patients, namely those with increased exacerbation risk plus higher blood eosinophil count (BEC), can benefit from ICS treatment. This review describes the components of inflammation modulated by ICS in COPD and the reasons for the variation in response to ICS between individuals. There are corticosteroid-insensitive inflammatory pathways in COPD, such as bacteria-induced macrophage interleukin-8 production and resultant neutrophil recruitment, but also corticosteroid-sensitive pathways including the reduction of type 2 markers and mast cell numbers. The review also describes the mechanisms whereby ICS can skew the lung microbiome, with reduced diversity and increased relative abundance, towards an excess of proteobacteria. BEC is a biomarker used to enable the selective use of ICS in COPD, but the clinical outcome in an individual is decided by a complex interacting network involving the microbiome and airway inflammation.

Identifiants

pubmed: 37852657
pii: 32/170/230084
doi: 10.1183/16000617.0084-2023
pmc: PMC10582931
pii:
doi:

Substances chimiques

Adrenal Cortex Hormones 0
Anti-Inflammatory Agents 0

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright ©The authors 2023.

Déclaration de conflit d'intérêts

Conflict of interest: D. Singh has received sponsorship to attend and speak at international meetings or honoraria for lecturing or attending advisory boards from Aerogen, AstraZeneca, Boehringer Ingelheim, Chiesi, Cipla, CSL Behring, Epiendo, Genentech, GlaxoSmithKline, Glenmark, Gossamerbio, Kinaset, Menarini, Novartis, Pulmatrix, Sanofi, Teva, Theravance and Verona. A. Beech, A. Higham and S. Lea have no conflicts of interest to declare.

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Auteurs

Simon Lea (S)

Division of Immunology, Immunity to Infection and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, The University of Manchester, Manchester, UK Simon.lea@manchester.ac.uk.

Andrew Higham (A)

Division of Immunology, Immunity to Infection and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, The University of Manchester, Manchester, UK.

Augusta Beech (A)

Division of Immunology, Immunity to Infection and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, The University of Manchester, Manchester, UK.

Dave Singh (D)

Division of Immunology, Immunity to Infection and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, The University of Manchester, Manchester, UK.
Medicines Evaluation Unit, Manchester University NHS Foundation Trust, Manchester, UK.

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