Abstract
Tonsil and adenoid-tissue hypertrophy (AH) is the most common cause of pediatric sleep-disordered breathing (SDB), with AH possibly initiated by repeated exposure to infectious agents or allergens. Here, we evaluated IL-17A activity in adenoid tissue from children with SDB and its association with AH and pneumococcal carriage. Thirty-five children (aged 3–12 years) with SDB and receiving adenoidectomy and tonsillectomy were enrolled. During surgery, nasopharyngeal carriage was determined by bacterial culture and multiplex PCR via nasopharyngeal swab, and adenoid samples were collected. IL-17A and associated cytokine expression was evaluated by real-time PCR and western blotting. The mRNA analysis showed that IL-17A level, IL-17A:IL-10 ratio, and RAR-related orphan receptor-γt:forkhead box P3 ratio were significantly higher in adenoid tissues with AH, as were IL-17A level and IL-17A:IL-10 ratio in adenoid tissues with pneumococcal carriage. Additionally, pneumococcal carriage was more common in nasopharyngeal adenoids from patients without AH than those with AH. IL-17A was upregulated in adenoid tissues from patients with AH and with pneumococcal carriage. These results suggested that pneumococcal carriage initiates an IL-17A-mediated immune response in nasopharyngeal adenoids, which might be associated with AH in patients with SDB.
Highlights
Obstructive sleep-disordered breathing (SDB) is a clinical condition associated with breathing problems due to an obstruction of the upper airways when sleeping and ranges in severity from simple snoring to obstructive sleep apnea syndrome (OSAS)[1,2]
We tested the hypothesis that Th17 cells and the associated immune response might play a role in S. pneumoniae scavenging and adenoid-tissue hypertrophy (AH) development by evaluating IL-17A expression in adenoid tissue from children with SDB and its association with AH and pneumococcal carriage
These results indicated that pneumococcal carriage might initiate IL-17A-mediated immune response in nasopharyngeal adenoids to eradicate colonization, and that this activity might be associated with AH in patients with SDB
Summary
Obstructive sleep-disordered breathing (SDB) is a clinical condition associated with breathing problems due to an obstruction of the upper airways when sleeping and ranges in severity from simple snoring to obstructive sleep apnea syndrome (OSAS)[1,2]. Regulatory T (Treg) cells expressing the transcription factor forkhead box P3 (Foxp3) play an important regulatory role during infections, diminish immune responses to microbial pathogens, and prevent inflammation-related local-tissue damage or autoimmunity, but are capable of contributing to infection chronicity[15,16]. Th17 cells expressing the transcription factor RAR-related orphan receptor-γt (RORγt) and its signature cytokine IL-17A play an important role in host defense against infection, including mucosal clearance of pneumococcal colonization[20,21,22]. We tested the hypothesis that Th17 cells and the associated immune response might play a role in S. pneumoniae scavenging and AH development by evaluating IL-17A expression in adenoid tissue from children with SDB and its association with AH and pneumococcal carriage
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