Leukotriene pathways and in vitro adenotonsillar cell proliferation in children with obstructive sleep apnea

Ehab Dayyat1, Laura D Serpero1, Leila Kheirandish-Gozal1

  • 1Department of Pediatrics, Division of Sleep Medicine and Kosair Children's Hospital Research Institute, University of Louisville, Louisville, KY.

Chest
|January 2, 2009
PubMed
Abstract

Insights

Leukotriene (LT) antagonists may treat obstructive sleep apnea (OSA) in children by reducing adenotonsillar cell proliferation and inflammation. These findings suggest potential non-surgical treatment options for pediatric OSA.

Area of Science:

  • Pediatric Pulmonology
  • Immunology
  • Pharmacology

Background:

  • Obstructive sleep apnea (OSA) in children is linked to high leukotriene (LT) expression in adenotonsillar tissues.
  • LT antagonists show potential as a therapeutic strategy for pediatric OSA.

Purpose of the Study:

  • To investigate the effects of LTD4 and LT receptor antagonists on adenotonsillar cell proliferation and inflammatory cytokine production in pediatric OSA.
  • To evaluate the efficacy of zileuton, montelukast, and BAY u9773 in modulating these cellular responses.

Main Methods:

  • Adenotonsillar cells from children with OSA were cultured and exposed to LTD4 and LT antagonists.
  • Cell proliferation was measured using [3H]-thymidine incorporation.
  • Inflammatory cytokine levels (TNF-alpha, IL-6, IL-8, IL-10, IL-12) were quantified via ELISA.

Main Results:

  • LTD4 significantly increased adenotonsillar cell proliferation.
  • Montelukast, BAY u9773, and zileuton dose-dependently reduced proliferation, with montelukast being most effective.
  • All antagonists decreased TNF-alpha, IL-6, and IL-12 levels, indicating anti-inflammatory effects.

Conclusions:

  • Leukotriene pathways are involved in the proliferation and inflammation of adenotonsillar tissues in pediatric OSA.
  • Targeting these LT pathways with antagonists offers a potential non-surgical approach for managing pediatric OSA.

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