4.6 Article

Nasopharyngeal metatranscriptome profiles of infants with bronchiolitis and risk of childhood asthma: a multicentre prospective study

Journal

EUROPEAN RESPIRATORY JOURNAL
Volume 60, Issue 1, Pages -

Publisher

EUROPEAN RESPIRATORY SOC JOURNALS LTD
DOI: 10.1183/13993003.02293-2021

Keywords

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Funding

  1. National Institutes of Health (NIH) [U01 AI-087881, R01 AI-114552, R01 AI-108588, R01 AI-134940, UG3/UH3 OD-023253]
  2. Margaret Q. Landenberger Research Foundation
  3. NIH National Center for Advancing Translational Sciences [UL1 TR-001876]
  4. Fundacao para a Ciencia e a Tegnologia [T495756868-00032862]

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Through transcriptome and clustering analysis, we identified biologically distinct metatranscriptome profiles with differential risks of asthma in infant bronchiolitis.
Background Bronchiolitis is not only the leading cause of hospitalisation in US infants but also a major risk factor for asthma development. Growing evidence supports clinical heterogeneity within bronchiolitis. Our objectives were to identify metatranscriptome profiles of infant bronchiolitis, and to examine their relationship with the host transcriptome and subsequent asthma development. Methods As part of a multicentre prospective cohort study of infants (age < 1 year) hospitalised for bronchiolitis, we integrated virus and nasopharyngeal metatranscriptome (species-level taxonomy and function) data measured at hospitalisation. We applied network-based clustering approaches to identify metatranscriptome profiles. We then examined their association with the host transcriptome at hospitalisation and risk for developing asthma. Results We identified five metatranscriptome profiles of bronchiolitis (n=244): profile A: virus(RSV )microbiome(commensals); profile B: virus(RSV/RV-A )microbiome(H.influenzae); profile C: virus(RSV )microbiome(S.pneumoniae); profile D: virus(RSV )microbiome(M.nonliquefaciens); and profile E: virus(RSV/RV-C) microbiome(M.catarrhalis). Compared with profile A, profile B infants were characterised by a high proportion of eczema, Haemophilus influenzae abundance and enriched virulence related to antibiotic resistance. These profile B infants also had upregulated T-helper 17 and downregulated type I interferon pathways (false discovery rate (FDR) < 0.005), and significantly higher risk for developing asthma (17.9% versus 38.9%; adjusted OR 2.81, 95% CI 1.11-7.26). Likewise, profile C infants were characterised by a high proportion of parental asthma, Streptococcus pneumoniae dominance, and enriched glycerolipid and glycerophospholipid metabolism of the microbiome. These profile C infants had an upregulated RAGE signalling pathway (FDR < 0.005) and higher risk of asthma (17.9% versus 35.6%; adjusted OR 2.49, 95% CI 1.10-5.87). Conclusions Metatranscriptome and clustering analysis identified biologically distinct metatranscriptome profiles that have differential risks of asthma.

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