AI Article Synopsis

  • Bronchiolitis is a leading cause of infant hospitalizations in the US and can increase the risk of asthma; this study aimed to identify distinct metatranscriptome profiles related to the condition.
  • Researchers examined metatranscriptome data of 244 infants hospitalized for bronchiolitis and identified five unique profiles, noting associations with the host transcriptome and asthma risk.
  • Profile B infants showed a significant increase in asthma risk and distinct immune pathway activity, while Profile C infants also had a high asthma risk linked to specific metabolic pathways.

Article Abstract

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: virusmicrobiome; profile B: virusmicrobiome ; profile C: virusmicrobiome ; profile D: virusmicrobiome ; and profile E: virusmicrobiome . Compared with profile A, profile B infants were characterised by a high proportion of eczema, 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% 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, 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% 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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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9206513PMC
http://dx.doi.org/10.1183/13993003.02293-2021DOI Listing

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