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Integrated omics endotyping of infants with respiratory syncytial virus bronchiolitis and risk of childhood asthma

Author

Listed:
  • Yoshihiko Raita

    (Massachusetts General Hospital, Harvard Medical School)

  • Marcos Pérez-Losada

    (The George Washington University
    Universidade do Porto, Campus Agrário de Vairão)

  • Robert J. Freishtat

    (Center for Genetic Medicine Research, Children’s National Hospital
    Children’s National Hospital
    George Washington University School of Medicine and Health Sciences)

  • Brennan Harmon

    (Center for Genetic Medicine Research, Children’s National Hospital)

  • Jonathan M. Mansbach

    (Harvard Medical School)

  • Pedro A. Piedra

    (Baylor College of Medicine)

  • Zhaozhong Zhu

    (Massachusetts General Hospital, Harvard Medical School)

  • Carlos A. Camargo

    (Massachusetts General Hospital, Harvard Medical School)

  • Kohei Hasegawa

    (Massachusetts General Hospital, Harvard Medical School)

Abstract

Respiratory syncytial virus (RSV) bronchiolitis is not only the leading cause of hospitalization in U.S. infants, but also a major risk factor for asthma development. While emerging evidence suggests clinical heterogeneity within RSV bronchiolitis, little is known about its biologically-distinct endotypes. Here, we integrated clinical, virus, airway microbiome (species-level), transcriptome, and metabolome data of 221 infants hospitalized with RSV bronchiolitis in a multicentre prospective cohort study. We identified four biologically- and clinically-meaningful endotypes: A) clinicalclassicmicrobiomeM. nonliquefaciensinflammationIFN-intermediate, B) clinicalatopicmicrobiomeS. pneumoniae/M. catarrhalisinflammationIFN-high, C) clinicalseveremicrobiomemixedinflammationIFN-low, and D) clinicalnon-atopicmicrobiomeM.catarrhalisinflammationIL-6. Particularly, compared with endotype A infants, endotype B infants—who are characterized by a high proportion of IgE sensitization and rhinovirus coinfection, S. pneumoniae/M. catarrhalis codominance, and high IFN-α and -γ response—had a significantly higher risk for developing asthma (9% vs. 38%; OR, 6.00: 95%CI, 2.08–21.9; P = 0.002). Our findings provide an evidence base for the early identification of high-risk children during a critical period of airway development.

Suggested Citation

  • Yoshihiko Raita & Marcos Pérez-Losada & Robert J. Freishtat & Brennan Harmon & Jonathan M. Mansbach & Pedro A. Piedra & Zhaozhong Zhu & Carlos A. Camargo & Kohei Hasegawa, 2021. "Integrated omics endotyping of infants with respiratory syncytial virus bronchiolitis and risk of childhood asthma," Nature Communications, Nature, vol. 12(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-23859-6
    DOI: 10.1038/s41467-021-23859-6
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    Cited by:

    1. Michimasa Fujiogi & Yoshihiko Raita & Marcos Pérez-Losada & Robert J. Freishtat & Juan C. Celedón & Jonathan M. Mansbach & Pedro A. Piedra & Zhaozhong Zhu & Carlos A. Camargo & Kohei Hasegawa, 2022. "Integrated relationship of nasopharyngeal airway host response and microbiome associates with bronchiolitis severity," Nature Communications, Nature, vol. 13(1), pages 1-12, December.
    2. Zhaozhong Zhu & Yijun Li & Robert J. Freishtat & Juan C. Celedón & Janice A. Espinola & Brennan Harmon & Andrea Hahn & Carlos A. Camargo & Liming Liang & Kohei Hasegawa, 2023. "Epigenome-wide association analysis of infant bronchiolitis severity: a multicenter prospective cohort study," Nature Communications, Nature, vol. 14(1), pages 1-13, December.

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