Th17/Treg balance in children with obstructive sleep apnea syndrome and the relationship with allergic rhinitis.

OBJECTIVE

This study aims to explore the role of the Th17 to Treg cell ratio in children with OSA and its relationship with allergic rhinitis.

METHODS

The study included 127 children diagnosed with OSA by polysomnography (PSG) testing and 29 children without OSA. The 127 children with OSA were divided into the following groups: OSA with moderate adenoidal hypertrophy (n=47), OSA with severe adenoidal hypertrophy (n=49), and OSA complicated by allergic rhinitis (AR) (n=31). The adenoids of the 29 children without OSA were mildly hypertrophic. We measured the number of Th17 and Treg cells, the levels of related serum cytokines in cellular secretions, and the expression of key transcription factors in both the peripheral blood and adenoid tissue. The Th17/Treg ratio was calculated and analyzed between groups. The numbers of Th17 and Treg cells were measured by flow cytometry; the secreted IL-17, IL-10, and TGF-β were measured by ELISA; and the expression levels of RORγt and Foxp3 were measured by RT-PCR.

RESULTS

Compared with the control group, OSA children exhibited a significant increase in the number of peripheral Th17 cells, Th17-related cytokine secretion (IL-17), and RORγt mRNA levels, whereas they exhibited a decrease in the number of Treg cells, Treg-related cytokine secretions (IL-10, TGF-β) and Foxp3 mRNA levels. The Th17/Treg ratio was higher (p<0.05) in the OSA groups than in the control group. The Th17/Treg ratio was correlated with the size of the adenoids. We also found that the Th17/Treg balance in OSA patients was complicated by allergic rhinitis; the increase was significantly larger in the AR group (p<0.05, p=0.021) than in OSA groups without AR. These results were observed in both the peripheral blood and local adenoid tissue.

CONCLUSION

The Th17/Treg imbalance may increase the risk of developing OSA, and AR may promote the development of the disease. These results provide an alternative explanation for OSA pathogenesis that warrants additional research and presents new directions for the prevention and treatment of OSA in children.