Relationship between inflammatory status and microbial composition in severe asthma and during exacerbation.


Journal

Allergy
ISSN: 1398-9995
Titre abrégé: Allergy
Pays: Denmark
ID NLM: 7804028

Informations de publication

Date de publication:
11 2022
Historique:
revised: 24 05 2022
received: 17 01 2022
accepted: 30 05 2022
pubmed: 2 7 2022
medline: 1 11 2022
entrez: 1 7 2022
Statut: ppublish

Résumé

In T2-mediated severe asthma, biologic therapies, such as mepolizumab, are increasingly used to control disease. Current biomarkers can indicate adequate suppression of T2 inflammation, but it is unclear whether they provide information about airway microbial composition. We investigated the relationships between current T2 biomarkers and microbial profiles, characteristics associated with a Proteobacteria Microbiota sequencing was performed on sputum samples obtained at stable and exacerbation state from 140 subjects with severe asthma participating in two clinical trials. Inflammatory subgroups were compared on the basis of biomarkers, including FeNO and sputum and blood eosinophils. Proteobacteria Microbial composition was not related to inflammatory subgroup based on sputum or blood eosinophils. FeNO ≥50 ppb when stable and at exacerbation indicated a group with less dispersed microbial profiles characterised by high alpha-diversity and low Proteobacteria. Proteobacteria High FeNO could indicate a subgroup of severe asthma less likely to benefit from antimicrobial strategies at exacerbation or in the context of poor control. Where FeNO is <50 ppb, biomarkers of microbial composition are required to identify those likely to respond to microbiome-directed strategies. We found no evidence that mepolizumab alters airway microbial composition.

Sections du résumé

BACKGROUND
In T2-mediated severe asthma, biologic therapies, such as mepolizumab, are increasingly used to control disease. Current biomarkers can indicate adequate suppression of T2 inflammation, but it is unclear whether they provide information about airway microbial composition. We investigated the relationships between current T2 biomarkers and microbial profiles, characteristics associated with a Proteobacteria
METHODS
Microbiota sequencing was performed on sputum samples obtained at stable and exacerbation state from 140 subjects with severe asthma participating in two clinical trials. Inflammatory subgroups were compared on the basis of biomarkers, including FeNO and sputum and blood eosinophils. Proteobacteria
RESULTS
Microbial composition was not related to inflammatory subgroup based on sputum or blood eosinophils. FeNO ≥50 ppb when stable and at exacerbation indicated a group with less dispersed microbial profiles characterised by high alpha-diversity and low Proteobacteria. Proteobacteria
CONCLUSION
High FeNO could indicate a subgroup of severe asthma less likely to benefit from antimicrobial strategies at exacerbation or in the context of poor control. Where FeNO is <50 ppb, biomarkers of microbial composition are required to identify those likely to respond to microbiome-directed strategies. We found no evidence that mepolizumab alters airway microbial composition.

Identifiants

pubmed: 35778780
doi: 10.1111/all.15425
doi:

Substances chimiques

Biomarkers 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

3362-3376

Subventions

Organisme : Medical Research Council
ID : G0801980
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/M016579/1
Pays : United Kingdom
Organisme : Department of Health
Pays : United Kingdom

Informations de copyright

© 2022 The Authors. Allergy published by European Academy of Allergy and Clinical Immunology and John Wiley & Sons Ltd.

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Auteurs

Sarah Diver (S)

Department of Respiratory Sciences, Leicester NIHR BRC, Institute for Lung Health, University of Leicester, Leicester, UK.

Koirobi Haldar (K)

Department of Respiratory Sciences, Leicester NIHR BRC, Institute for Lung Health, University of Leicester, Leicester, UK.

Pamela Jane McDowell (PJ)

Wellcome-Wolfson Centre for Experimental Medicine, School of Medicine, Dentistry, and Biological Sciences, Belfast, UK.
Queen's University Belfast, Belfast, UK.

John Busby (J)

Wellcome-Wolfson Centre for Experimental Medicine, School of Medicine, Dentistry, and Biological Sciences, Belfast, UK.
Queen's University Belfast, Belfast, UK.

Vijay Mistry (V)

Department of Respiratory Sciences, Leicester NIHR BRC, Institute for Lung Health, University of Leicester, Leicester, UK.

Claudia Micieli (C)

Department of Respiratory Sciences, Leicester NIHR BRC, Institute for Lung Health, University of Leicester, Leicester, UK.

Vanessa Brown (V)

Wellcome-Wolfson Centre for Experimental Medicine, School of Medicine, Dentistry, and Biological Sciences, Belfast, UK.
Queen's University Belfast, Belfast, UK.

Ciara Cox (C)

Regional Virus Laboratory, Royal Victoria Hospital, Belfast Health and Social Care Trust, Belfast, UK.

Freda Yang (F)

Division of Immunology, Infection and Inflammation, University of Glasgow, Glasgow, UK.

Catherine Borg (C)

Oxford Respiratory NIHR BRC, Nuffield Department of Medicine, University of Oxford, Oxford, UK.

Rahul Shrimanker (R)

Oxford Respiratory NIHR BRC, Nuffield Department of Medicine, University of Oxford, Oxford, UK.

Mohammadali Yavari Ramsheh (MY)

Department of Respiratory Sciences, Leicester NIHR BRC, Institute for Lung Health, University of Leicester, Leicester, UK.

Tim Hardman (T)

Niche Science & Technology Ltd., Unit 26, Falstaff House, Richmond, UK.

Joseph Arron (J)

Genentech Inc., South San Francisco, California, USA.

Peter Bradding (P)

Department of Respiratory Sciences, Leicester NIHR BRC, Institute for Lung Health, University of Leicester, Leicester, UK.

Douglas Cowan (D)

NHS Greater Glasgow and Clyde, Stobhill Hospital, Glasgow, UK.

Adel Hasan Mansur (AH)

University of Birmingham and Heartlands Hospital, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK.

Stephen J Fowler (SJ)

Division of Infection, Immunity and Respiratory Medicine, School of Biological Sciences, The University of Manchester, Manchester, UK.
Manchester Academic Health Science Centre and NIHR Manchester Biomedical Research Centre, Manchester University Hospitals NHS Foundation Trust, Manchester, UK.

Jim Lordan (J)

The Newcastle upon Tyne NHS Foundation Trust, Newcastle upon Tyne, UK.

Andrew Menzies-Gow (A)

Royal Brompton & Harefield Hospitals, London, UK.

Douglas Robinson (D)

University College Hospitals NHS Foundation Trust, London, UK.

John Matthews (J)

Department of Respiratory Sciences, Leicester NIHR BRC, Institute for Lung Health, University of Leicester, Leicester, UK.
23andMe, Sunnyvale, California, USA.

Ian D Pavord (ID)

Oxford Respiratory NIHR BRC, Nuffield Department of Medicine, University of Oxford, Oxford, UK.

Rekha Chaudhuri (R)

Division of Immunology, Infection and Inflammation, University of Glasgow, Glasgow, UK.

Liam G Heaney (LG)

Wellcome-Wolfson Centre for Experimental Medicine, School of Medicine, Dentistry, and Biological Sciences, Belfast, UK.
Queen's University Belfast, Belfast, UK.

Michael R Barer (MR)

Department of Respiratory Sciences, Leicester NIHR BRC, Institute for Lung Health, University of Leicester, Leicester, UK.

Christopher Brightling (C)

Department of Respiratory Sciences, Leicester NIHR BRC, Institute for Lung Health, University of Leicester, Leicester, UK.

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