Expression of chitinases in hypertrophied adenoids of children

Kyung Wook Heo1, Dae Young Hur, Seong Kook Park

  • 1Department of Otorhinolaryngology-Head & Neck Surgery, Inje University College of Medicine, Busan Paik Hospital, Busan, Republic of Korea.

Insights

Acidic mammalian chitinase (AMCase) and chitotriosidase (ChT) are overexpressed in children with hypertrophied adenoids linked to chronic rhinosinusitis (CRS), otitis media with effusion (OME), and allergic rhinitis (AR). This suggests a role for chitinases in these common pediatric conditions.

Area of Science:

  • Immunology
  • Otolaryngology
  • Molecular Biology

Background:

  • Chronic rhinosinusitis (CRS), otitis media with effusion (OME), and allergic rhinitis (AR) are prevalent pediatric conditions often linked to adenoid hypertrophy.
  • Adenoidectomy is a common clinical intervention for these conditions.

Purpose of the Study:

  • To investigate the expression levels and cellular localization of acidic mammalian chitinase (AMCase) and chitotriosidase (ChT) in hypertrophied adenoids.
  • To determine the relationship between AMCase and ChT expression and the presence of CRS, OME, and AR in children.

Main Methods:

  • Prospective cohort study involving 41 children undergoing adenoidectomy.
  • Analysis of adenoid tissue for mRNA and protein expression of AMCase and ChT using RT-PCR and Western blotting.
  • Immunohistochemical staining to identify the specific cell types expressing AMCase and ChT.

Main Results:

  • Both AMCase and ChT were detected at mRNA and protein levels in all adenoid samples.
  • Expression of AMCase was significantly associated with CRS.
  • Expression of ChT was significantly associated with CRS, OME, and AR.
  • AMCase and ChT were primarily expressed in histiocytes and vascular endothelial cells.

Conclusions:

  • Overexpression of AMCase and ChT in hypertrophied adenoids may contribute to CRS, OME, and AR in children.
  • Chitin-containing pathogens or aberrant immune responses to them are implicated.
  • These findings highlight a potential molecular mechanism underlying these common pediatric airway inflammatory diseases.
Abstract

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