Background: Obstructive sleep apnea syndrome (OSAS) is characterized by a majority population of respiratory sleep disorders, which consists of simple snoring as well as increased upper airway resistance syndrome. Adenoid hypertrophy has been suggested as the main cause of OSAS in children. The role of interleukin-33 (IL-33) and its receptor suppressor of tumorigenicity 2 (ST2) in a variety of pediatric allergic diseases has been confirmed. We hypothesized that IL-33/ST2 path way might play a pivotal role in the pathogenesis of adenoid hypertrophy-associated OSAS in children.
Methods: A total of 40 children undergoing adenoidectomy due to OSAS in the Otolaryngology of Tianjin Children's Hospital were selected as the study participants. The quantity of IL-33 and ST2 positive cells in adenoids was detected by immunohistochemical (IHC) streptavidin-peroxidase conjugate (SP) method.
Results: The IL-33 positive cells were mainly distributed in the submucosa epithelium and vascular endothelium, and expressed in the nucleus and cytoplasm. Meanwhile, ST2 positive cells were primarily observed in the mucosa and expressed in the nucleus and cytoplasm, with a little expression of intercellular substance. There was a positive correlation between the proportion of adenoids in the posterior nostril diameter and the number of IL-33 positive cells. The expression of IL-33 in adenoids was positively correlated with the level of ST2 (r=0.809, P=0.000). The expression of IL-33 in adenoids was positively correlated with the level of eosinophil granulocyte (r=0.859, P=0.000). Moreover, the expression of ST2 in adenoids was positively correlated with the level of eosinophil granulocyte (r=0.814, P=0.000). The number of IL-33 positive cells was significantly higher in the moderate hypoxemia group than that in the mild hypoxemia group (P<0.05). There was no significant difference in the number of ST2 positive cells between the moderate hypoxemia group and mild hypoxemia group (P>0.05).
Conclusions: Both IL-33 and its receptor ST2 were expressed in adenoids of OSAS children. The severity of airway obstruction caused by adenoid hypertrophy was positively correlated with the expression of IL-33.
Keywords: Children; adenoidal hypertrophy; interleukin-33 (IL-33); obstructive sleep apnea syndrome (OSAS); suppressor of tumorigenicity 2 (ST2).
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