Compared to profile A, infants with bronchiolitis metatranscriptome profile B had a significantly higher risk of developing asthma (38.9% vs 17.9%; adjusted OR 2.81, 95% CI 1.11-7.26).
Cohort (n=244)
Yes
Do specific nasopharyngeal metatranscriptome profiles in infants hospitalized with bronchiolitis predict the risk of developing childhood asthma?
Biologically distinct nasopharyngeal metatranscriptome profiles in infants with bronchiolitis are associated with differential risks of developing childhood asthma.
Odds Ratio: 2.81 (95% CI 1.11–7.26)
Absolute Event Rate: 38.9% vs 17.9%
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.
Raita et al. (Thu,) conducted a cohort in Bronchiolitis (n=244). Metatranscriptome profile B (virus RSV/RV-A microbiome H.influenzae) vs. Metatranscriptome profile A (virus RSV microbiome commensals) was evaluated on Risk for developing asthma (adjusted OR 2.81, 95% CI 1.11-7.26). Compared to profile A, infants with bronchiolitis metatranscriptome profile B had a significantly higher risk of developing asthma (38.9% vs 17.9%; adjusted OR 2.81, 95% CI 1.11-7.26).