Enhancement of YKL40,IL-6,IL-8, TNF-a, and the possible mechanism of YKL40 promoting overexpression of IL-6,IL-8, TNF-a in childhood with obstructive sleep apnea syndrome

Abstract

AbstractObjective To evaluate the levels of YKL40, IL-6(interleukin-6), IL-8(interleukin-8), IL-10(interleukin-10), TNF-a (tumor necrosis factor-α) in OSAS (obstructive sleep apnea syndrome )children and explore the mechanism of YKL40 promoting inflammatory factors overexpression in tonsils. Methods qPCR and ELISA were used to identify the expression of YKL40, IL-6, IL-8, IL-10, and TNF-a in the tonsils of OSAS children. Primary tonsil lymphocytes (PTLCs) were cultured and recombinant human YKL40(rhYKL40)was used to stimulate PTLCs in different concentrations and time points. The activation of NF-κb in PTLCs was observed by western blotting. Results Relative mRNA of YKL40, IL-6, IL-8, TNF-α was overexpression in OSAS-derived tonsil tissue and the levels of YKL40, IL-6, IL-8, and TNF-α increased in OSAS-derived tonsil protein supernatant.The relative mRNA expression of IL-6, IL-8 and TNF-α were increased under the treatment of YKL40 (100 ng/mmol for 24h). The phosphorylation of NF-κb p65 was stimulated in the process. Conclusion The levels of YKL40, IL-6, IL-8, and TNF-α increased in OSAS children, and YKL40 may promote the overexpression of IL-6, IL-8 and TNF-α in PTLCs via NF-κb pathway. This result indicates that inflammation may play an important role in the pathogenesis of OSAS in children. Inhibition of YKL40 may have a potential therapeutic target for YKL40-induced inflammation in pediatric OSAS.