Department of Otorhinolaryngology, The First Affiliated Hospital, Fujian Medical University, Chazhong Road 20th, Fuzhou, 350000, China.
Department of Otorhinolaryngology, Binhai Campus of the First Affiliated Hospital, National Regional Medical Center, Fujian Medical University, Fuzhou, 350212, China.
Sci Rep. 2024 Nov 1;14(1):26283. doi: 10.1038/s41598-024-74402-8.
To evaluate the levels of YKL40, IL-6(interleukin-6), IL-8(interleukin-8), IL-10(interleukin-10), TNF-α (tumor necrosis factor-α) in OSAS (obstructive sleep apnea syndrome)children and explore the mechanism of YKL40 promoting inflammatory factors overexpression in tonsils. qPCR and ELISA were used to identify the expression of YKL40, IL-6, IL-8, IL-10, and TNF-α 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 at different time points. The activation of NF-κB in PTLCs was screened by western blotting. Relative mRNA of YKL40, IL-6, IL-8, TNF-α was over expressed in OSAS-derived tonsil tissue and the levels of YKL40, IL-6, IL-8, and TNF-α was increased in OSAS-derived protein supernatant of tonsil tissue.The relative mRNA expression of IL-6, IL-8 and TNF-α increased under the treatment of YKL40 (100 ng/mmol for 24 h). The phosphorylation of p65 in NF-κB pathway was stimulated in the process. The levels of YKL40, IL-6, IL-8, and TNF-α increases in OSAS children, and YKL40 promotes the overexpression of IL-6, IL-8 and TNF-α in PTLCs via NF-κB pathway. The result implements that inflammation may play an important role in the pathogenesis of OSAS in children.
评估 YKL40、IL-6(白细胞介素-6)、IL-8(白细胞介素-8)、IL-10(白细胞介素-10)和 TNF-α(肿瘤坏死因子-α)在阻塞性睡眠呼吸暂停综合征(OSAS)患儿中的水平,并探讨 YKL40 促进扁桃体中炎症因子过度表达的机制。
采用 qPCR 和 ELISA 法检测 OSAS 患儿扁桃体组织中 YKL40、IL-6、IL-8、IL-10 和 TNF-α 的表达。培养原代扁桃体淋巴细胞(PTLCs),并采用不同浓度和时间点的重组人 YKL40(rhYKL40)刺激 PTLCs。采用 Western blot 法筛选 PTLCs 中 NF-κB 的激活情况。OSAS 来源的扁桃体组织中 YKL40、IL-6、IL-8 和 TNF-α 的相对 mRNA 表达过度,OSAS 来源的扁桃体组织上清液中 YKL40、IL-6、IL-8 和 TNF-α 的水平升高。YKL40(100ng/mmol,24h)处理后,IL-6、IL-8 和 TNF-α 的相对 mRNA 表达增加,NF-κB 通路中 p65 的磷酸化受到刺激。OSAS 患儿 YKL40、IL-6、IL-8 和 TNF-α 水平升高,YKL40 通过 NF-κB 通路促进 PTLCs 中 IL-6、IL-8 和 TNF-α 的过度表达。
结果表明,炎症可能在儿童 OSAS 的发病机制中起重要作用。