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Published on: August 7, 2017
Effect of fluticasone furoate on interleukin 6 secretion from adenoid tissues in children with obstructive sleep
Rania Esteitie1, Janaki Emani, Shilpy Sharma
1Section of Otolaryngology-Head and Neck Surgery, The University of Chicago Medical Center, IL 60637, USA.
Insights
Intranasal corticosteroid therapy reduced the proinflammatory cytokine IL-6 in adenoid tissue of children with obstructive sleep apnea syndrome. This finding suggests a potential mechanism for how these nasal sprays help treat childhood sleep apnea.
Area of Science:
- Pediatric Otolaryngology
- Immunology
- Sleep Medicine
Background:
- Obstructive sleep apnea syndrome (OSAS) in children is associated with inflammation in adenoid tissues.
- T-regulatory cells and cytokines play a role in the inflammatory processes of OSAS.
Purpose of the Study:
- To investigate the impact of intranasal corticosteroid therapy on T-regulatory cells and inflammatory cytokines in the adenoid tissue of children diagnosed with OSAS.
- To assess whether fluticasone furoate nasal spray affects key inflammatory markers.
Main Methods:
- A randomized, prospective study involving 24 children (ages 2-12) with OSAS undergoing adenotonsillectomy.
- Participants received either fluticasone furoate nasal spray or no treatment for two weeks prior to surgery.
- Adenoid tissue was analyzed for T-regulatory cells (FOXP3, CD4, CD25) and cytokines (IL-10, IL-6, TGF-β).
Main Results:
- Fluticasone furoate nasal spray treatment led to a significant reduction in spontaneous and stimulated IL-6 release from adenoid tissue.
- No significant differences were observed in the counts of T-regulatory cells (CD4/FOXP3, CD25/FOXP3) or transforming growth factor-β.
- Immunohistochemical staining for IL-10 showed comparable results between the treated and untreated groups.
Conclusions:
- Intranasal fluticasone furoate therapy effectively reduces the proinflammatory cytokine IL-6 in adenoid tissue of children with OSAS.
- This reduction in IL-6 may contribute to the observed clinical benefits of intranasal corticosteroids in managing childhood obstructive sleep apnea syndrome.
Objective:
To determine the effect of intranasal corticosteroid therapy on T-regulatory cells and other inflammatory cytokines in adenoid tissues in children with obstructive sleep apnea syndrome.
Design:
Randomized, prospective, exploratory study.
Setting:
Academic pediatric otolaryngology practice in a tertiary care children's hospital.
Patients:
Participants included 24 children between the ages of 2 and 12 years who were undergoing adenotonsillectomy for polysomnogram-documented obstructive sleep apnea syndrome.
Intervention:
Children were randomized to either no treatment (n = 13) or treatment with fluticasone furoate nasal spray, 55 μg/nostril daily (n = 11), for 2 weeks before adenotonsillectomy. Adenoid tissue was obtained at the time of the procedure.
Main Outcome Measures:
The number of tissue T-regulatory cells, as determined by staining with FOXP3, CD4, and CD25, was the primary outcome measure. Staining for interleukin (IL)-10 and transforming growth factor-β protein by immunohistochemistry, and adenoid mononuclear cell spontaneous and induced release of cytokines (IL-10, IL-6, IL-12, IL-13, tumor necrosis factor, and transforming growth factor β) were secondary outcomes.
Results:
Cells isolated from fluticasone furoate nasal spray-treated adenoid tissue released significantly less IL-6 spontaneously as well as upon stimulation with anti-CD3 monoclonal antibody (P = .05) compared with nontreated adenoid tissue. There were no significant differences in the number of CD4/FOXP3-, CD25/FOXP3-, or transforming growth factor β-positive cells. Intensity of staining for IL-10 was also comparable between the groups.
Conclusions:
In this study, we show reduction of IL-6, a proinflammatory cytokine, in adenoid tissue obtained from children with obstructive sleep apnea syndrome treated with fluticasone furoate nasal spray. This reduction could contribute to the clinical efficacy of this class of medications in the treatment of childhood obstructive sleep apnea syndrome.
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