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IL-17A expression in the adenoid tissue from children with sleep disordered breathing and its association with

Chien-Chia Huang1,2, Pei-Wen Wu1,3, Chyi-Liang Chen4

  • 1Division of Rhinology, Department of Otolaryngology, Chang Gung Memorial Hospital and Chang Gung University, Taoyuan, Taiwan.

Scientific Reports
|November 15, 2018
PubMed

Insights

Pneumococcal carriage may trigger an IL-17A immune response in adenoid tissue, potentially causing hypertrophy (AH) in children with sleep-disordered breathing (SDB). This immune response is linked to AH development in SDB patients.

Area of Science:

  • Immunology
  • Pediatrics
  • Otolaryngology

Background:

  • Tonsil and adenoid hypertrophy (AH) is a primary cause of pediatric sleep-disordered breathing (SDB).
  • Infectious agents or allergens may initiate AH.
  • The role of IL-17A in AH and its association with pneumococcal carriage in SDB patients is not fully understood.

Purpose of the Study:

  • To evaluate IL-17A activity in adenoid tissue from children with SDB.
  • To investigate the association between IL-17A, AH, and pneumococcal carriage.
  • To explore the immune response mechanisms in AH.

Main Methods:

  • Adenoid tissue samples were collected from 35 children (aged 3-12 years) undergoing adenoidectomy and tonsillectomy for SDB.
  • Nasopharyngeal carriage was assessed using bacterial culture and multiplex PCR.
  • IL-17A and related cytokine expression was analyzed via real-time PCR and western blotting.

Main Results:

  • Elevated IL-17A levels and IL-17A:IL-10 ratios were observed in adenoid tissues with AH and pneumococcal carriage.
  • Pneumococcal carriage was more prevalent in patients without AH.
  • IL-17A upregulation correlated with AH and pneumococcal carriage in adenoid tissues.

Conclusions:

  • Pneumococcal carriage appears to initiate an IL-17A-mediated immune response in nasopharyngeal adenoids.
  • This IL-17A response may be associated with the development of AH in children with SDB.
  • Further research is warranted to elucidate the precise mechanisms linking pneumococcal carriage, IL-17A, and AH in pediatric SDB.

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