Bacterial communities co-develop with respiratory immunity early in life, linking dysbiosis to systemic monocyte signature and wheezing

Early microbial colonization influences respiratory disease risk, yet mechanisms remain unclear. In a prospective birth cohort of 256 infants, we profiled bacterial, fungal, and viral communities in the upper airway and assessed local immune gene expression longitudinally and systemic gene expression at 1 year. Bacterial populations, not fungal or viral, correlated most strongly with immune development during the first 3 months, coinciding with composition shifts and immune-related gene expression changes, including interferon and adaptive immunity pathways. In contrast, the mycobiome and resident viruses showed no significant coevolution with host immunity. By 1 year, infants who previously wheezed displayed an upper airway microbiota enriched in <i>Haemophilus influenzae</i> and <i>Moraxella</i>, accompanied by a distinct local and systemic immune gene signature featuring elevated classical monocyte-related genes. These findings reveal a specific link between early-life bacterial dysbiosis, monocyte-related immunity, and wheezing onset, suggesting potential targets for early intervention in respiratory disease.

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Publication Details

Journal
Science Advances
Published
2025-10-17
DOI
https://doi.org/10.1126/sciadv.adw1410
Citations
3
Primary Topic
Gut microbiota and health
Type
article
Field-Weighted Citation Impact
2.42

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article

Bacterial communities co-develop with respiratory immunity early in life, linking dysbiosis to systemic monocyte signature and wheezing

Céline Pattaroni, Mindy Gore, Matthew Macowan, Sejal Saglani et al.
3 citations
Science Advances
Gut microbiota and health
2.42
article

Bacterial communities co-develop with respiratory immunity early in life, linking dysbiosis to systemic monocyte signature and wheezing

Céline Pattaroni, Mindy Gore, Matthew Macowan, Sejal Saglani, Adnan Ćustović, Steve Turner, Jürgen Schwarze, Ultan F. Power, Bailey Cardwell, Jonathan Grigg, Andrew Bush, Graham Roberts, Peter Ghazal, Benjamin J. Marsland, Roxanne Chatzis, Clare M. Lloyd, Michael D. Shields, Giuseppe Iacono
article en
3 citations

Abstract

Early microbial colonization influences respiratory disease risk, yet mechanisms remain unclear. In a prospective birth cohort of 256 infants, we profiled bacterial, fungal, and viral communities in the upper airway and assessed local immune gene expression longitudinally and systemic gene expression at 1 year. Bacterial populations, not fungal or viral, correlated most strongly with immune development during the first 3 months, coinciding with composition shifts and immune-related gene expression changes, including interferon and adaptive immunity pathways. In contrast, the mycobiome and resident viruses showed no significant coevolution with host immunity. By 1 year, infants who previously wheezed displayed an upper airway microbiota enriched in <i>Haemophilus influenzae</i> and <i>Moraxella</i>, accompanied by a distinct local and systemic immune gene signature featuring elevated classical monocyte-related genes. These findings reveal a specific link between early-life bacterial dysbiosis, monocyte-related immunity, and wheezing onset, suggesting potential targets for early intervention in respiratory disease.

Science AdvancesVol. 11(42)
Queen's University Belfast (GB), Queen Mary University of London (GB), University of Aberdeen (GB), University Hospital Southampton NHS Foundation Trust (GB), NHS Grampian (GB), Royal Brompton Hospital (GB), Lung Institute (US), NIHR Imperial Biomedical Research Centre (GB), NIHR Southampton Biomedical Research Centre (GB), St Mary's Hospital (GB), David Hide Asthma and Allergy Research Centre (GB), Centre for Inflammation Research (GB), St. Mary's Hospital (GB), University of Southampton (GB), Imperial College London (GB), Monash University (AU), Cardiff University (GB), University of Edinburgh (GB)
Queen's University Belfast, Queen's University
Openalex Percentile: Top 10%
Gut microbiota and health
2.42
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