DOI: 10.1111/all.70481 ISSN: 0105-4538

Pathogenic Airway Bacteria and Local Immune Responses During Early‐Life Asthma‐Like Episodes

Mathilde Bundgaard Svendsen, Tamo Sultan, Anton Kjellberg, Mathias Melgaard, Susanne Brix, Karen Krogfelt, Nilo Vahman, Ann‐Marie Malby Schoos, Jakob Stokholm, Bo Lund Chawes, Klaus Bønnelykke, Jonathan Thorsen, Julie Nyholm Kyvsgaard

ABSTRACT

Background

Respiratory tract colonization by the pathogenic airway bacteria Haemophilus influenzae , Streptococcus pneumoniae , and/or Moraxella catarrhalis has been linked to the pathogenesis of childhood asthma and exacerbations, but the underlying mechanisms remain unclear.

Objective

To investigate the association of H. influenzae , S. pneumoniae , and M. catarrhalis with airway immune responses during acute early‐life asthma‐like episodes and examine how these responses differ between children with and without asthma.

Methods

The study included 476 asthma‐like episodes from 271 children aged 0 to 4 years from the COPSAC 2010 mother–child cohort. Levels of 17 immune mediators covering Type‐1, −2, and −17 and regulatory pathways were assessed in upper airway mucosal lining fluid while hypopharyngeal aspirates were collected for bacterial cultures and nasopharyngeal aspirates for viral PCR. Asthma was prospectively assessed until age 6 years.

Results

Detection of H. influenzae during asthma‐like symptoms was associated with elevated IL‐1β, TNF‐α, and IL‐2, alongside decreased CXCL10 levels. Similar immune profiles were observed in children with and without asthma by age 3. Detection of S. pneumoniae and M. catarrhalis were not associated with significant changes in immune mediator levels; however, children with asthma by age 3 exhibited elevated IL‐1β levels during detection of S. pneumoniae , a pattern not observed in children without asthma. No significant differences in mediator levels were observed in children with and without asthma at age 6.

Conclusion

Children with pathogenic bacterial detection in the airways during acute asthma‐like episodes exhibit an increased proinflammatory immune response marked by increased IL‐1β, IL‐2 and TNF‐α, which may promote chronic inflammation, possibly contributing to asthma development and exacerbations.

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