Evidence map›Paper›PMID 39127908›Full record

ArticleAllergy2024

Species-level, metagenomic and proteomic analysis of microbe-immune interactions in severe asthma.

Maisha F Jabeen, Nicholas D Sanderson, Mariaenrica Tinè, Gillian Donachie, Clair Barber, Adnan Azim, Laurie C K Lau, Thomas Brown, Ian D Pavord, Anoop Chauhan and 5 more

Abstract read
In one paragraph

Article in Allergy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Asthma endotypes and theratypes.Chinese medical journal pulmonary and critical care medicine · 2026
    Review
  4. Article
  5. Review
  6. Association of Childhood Asthma with the Concept of Exposomics: A Short Review.Medical science monitor : international medical journal of experimental and clinical research · 2025
    Review
  7. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors.

Maisha F JabeenNuffield Department of Medicine, Experimental Medicine Division, Respiratory Medicine Unit, John Radcliffe Hospital, University of Oxford, Oxford, UK.ORCID 0000-0002-1887-596X
Nicholas D SandersonNuffield Department of Clinical Medicine, John Radcliffe Hospital, University of Oxford, Oxford, UK.ORCID 0000-0001-6370-1961
Mariaenrica TinèDepartment of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padova, Padova, Italy.ORCID 0000-0002-3094-5721
Gillian DonachieNuffield Department of Medicine, Experimental Medicine Division, Respiratory Medicine Unit, John Radcliffe Hospital, University of Oxford, Oxford, UK.ORCID 0000-0002-8873-6455
Clair BarberClinical and Experimental Sciences, University of Southampton Faculty of Medicine, Sir Henry Wellcome Laboratories and NIHR Southampton Respiratory Biomedical Research Unit, Southampton University, Southampton, UK.ORCID 0000-0001-5335-5129
Adnan AzimClinical and Experimental Sciences, University of Southampton Faculty of Medicine, Sir Henry Wellcome Laboratories and NIHR Southampton Respiratory Biomedical Research Unit, Southampton University, Southampton, UK.ORCID 0000-0001-5960-1159
Laurie C K LauClinical and Experimental Sciences, University of Southampton Faculty of Medicine, Sir Henry Wellcome Laboratories and NIHR Southampton Respiratory Biomedical Research Unit, Southampton University, Southampton, UK.ORCID 0000-0002-5851-3867
Thomas BrownPortsmouth Hospitals NHS Trust, Portsmouth, UK.ORCID 0000-0001-7336-4719
Ian D PavordNuffield Department of Medicine, Experimental Medicine Division, Respiratory Medicine Unit, John Radcliffe Hospital, University of Oxford, Oxford, UK.ORCID 0000-0002-4288-5973
Anoop ChauhanPortsmouth Hospitals NHS Trust, Portsmouth, UK.ORCID 0000-0003-4044-6114
Paul KlenermanNuffield Department of Clinical Medicine, John Radcliffe Hospital, University of Oxford, Oxford, UK.ORCID 0000-0003-4307-9161
Teresa L StreetNuffield Department of Clinical Medicine, John Radcliffe Hospital, University of Oxford, Oxford, UK.ORCID 0000-0001-8491-240X
Emanuele MarchiNuffield Department of Medicine, Experimental Medicine Division, Respiratory Medicine Unit, John Radcliffe Hospital, University of Oxford, Oxford, UK.ORCID 0000-0003-1741-9353
Peter H HowarthClinical and Experimental Sciences, University of Southampton Faculty of Medicine, Sir Henry Wellcome Laboratories and NIHR Southampton Respiratory Biomedical Research Unit, Southampton University, Southampton, UK.ORCID 0000-0003-0619-7927
Timothy S C HinksNuffield Department of Medicine, Experimental Medicine Division, Respiratory Medicine Unit, John Radcliffe Hospital, University of Oxford, Oxford, UK.ORCID 0000-0003-0699-2373

Funding

Medical Research CouncilNational Institute for Health Research Southampton Biomedical Research CentreNIHR Oxford Biomedical Research CentreNIHR Primary Care Research NetworkWellcome Trust 211050Wellcome Trust 211050/Z/18/Z
6 · The paper itself

Abstract

backgroundThe airway microbiome in severe asthma has not been characterised at species-level by metagenomic sequencing, nor have the relationships between specific species and mucosal immune responses in 'type-2 low', neutrophilic asthma been defined. We performed an integrated species-level metagenomic data with inflammatory mediators to characterise prevalence of dominant potentially pathogenic organisms and host immune responses.

methodsSputum and nasal lavage samples were analysed using long-read metagenomic sequencing with Nanopore and qPCR in two cross-sectional adult severe asthma cohorts, Wessex (n = 66) and Oxford (n = 30). We integrated species-level data with clinical parameters and 39 selected airway proteins measured by immunoassay and O-link.

resultsThe sputum microbiome in health and mild asthma displayed comparable microbial diversity. By contrast, 23% (19/81) of severe asthma microbiomes were dominated by a single respiratory pathogen, namely H. influenzae (n = 10), M. catarrhalis (n = 4), S. pneumoniae (n = 4) and P. aeruginosa (n = 1). Neutrophilic asthma was associated with H. influenzae, M. catarrhalis, S. pneumoniae and T. whipplei with elevated type-1 cytokines and proteases; eosinophilic asthma with higher M. catarrhalis, but lower H. influenzae, and S. pneumoniae abundance. H. influenzae load correlated with Eosinophil Cationic Protein, elastase and IL-10. R. mucilaginosa associated positively with IL-6 and negatively with FGF. Bayesian network analysis also revealed close and distinct relationships of H. influenzae and M. catarrhalis with type-1 airway inflammation. The microbiomes and cytokine milieu were distinct between upper and lower airways.

conclusionsThis species-level integrated analysis reveals central, but distinct associations between potentially pathogenic bacteria and airways inflammation in severe asthma.

Indexed as

AsthmaMetagenomicsMicrobiotaProteomicsAdultCross-Sectional StudiesCytokinesFemaleHumansMaleMetagenomeMiddle AgedSeverity of Illness IndexSputumCytokinesAsthmabacteriacytokinemicrobiomesputum

Identifiers

PMID39127908
PMCPMC7617782

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.