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Sphingosine signaling dysfunction in airway cells as a potential contributor to progression from protracted bacterial

Sandra Hodge1,2, Matthew Macowan1,2, Hong Liu1,2

  • 1Lung Research Unit, Department of Thoracic Medicine, Royal Adelaide Hospital, Adelaide, South Australia, Australia.

Pediatric Pulmonology
|March 17, 2020
PubMed

Insights

Children with protracted bacterial bronchitis (PBB) and bronchiectasis (BE) show similar sphingosine-1-phosphate (S1P) pathway gene expression changes in alveolar macrophages. This suggests dysregulated S1P signaling contributes to airway inflammation and impaired macrophage function in these pediatric lung conditions.

Area of Science:

  • Pediatric Pulmonology
  • Immunology
  • Molecular Biology

Background:

  • Protracted bacterial bronchitis (PBB) may precede bronchiectasis (BE) in children.
  • Alveolar macrophages (AM) in children with PBB or BE exhibit phagocytic defects and inflammation.
  • Sphingosine-1-phosphate (S1P) signaling dysregulation is implicated in adult inflammatory lung diseases.

Purpose of the Study:

  • To investigate the role of S1P signaling pathway gene expression in pediatric PBB and BE.
  • To determine if S1P pathway dysregulation contributes to AM dysfunction in these conditions.

Main Methods:

  • Gene expression analysis using Custom TaqMan OpenArray in bronchoalveolar lavage samples from children with BE, PBB, and controls.
  • Investigated S1P-generating enzymes (SPHK, SGPP2, SGPL1), S1P receptors (S1PR), cytokines (TNF, IFNG), GZMB, and inflammasomes (AIM2, NLRP3).
  • Correlated gene expression with clinical data and airway inflammation.

Main Results:

  • Increased S1PR1, S1PR2, and SPHK1 expression in AM from both PBB and BE groups compared to controls.
  • Elevated SGPP2 in PBB AM only; increased TNF, IFNG, AIM2, and NLRP3 in both PBB and BE groups.
  • Significant associations found between bacterial growth, S1P mediators, and inflammatory markers.

Conclusions:

  • Children with PBB and BE share comparable S1P-associated gene expression profiles in AM.
  • Dysregulated S1P signaling is a likely mechanism underlying AM phagocytic dysfunction and inflammation in pediatric PBB and BE.
Abstract

Keywords:
Haemophilus influenzaebronchiectasischildhood lung diseaseinflammationphagocytosisprotracted bacterial bronchitissphingosine-1-phosphate (S1P)

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