论文部分内容阅读
目的建立肺炎链球菌性急性中耳炎小鼠模型,研究白细胞介素17A(interleukin 17A,IL-17A)促进中耳上皮细胞凋亡以及凋亡促进中耳组织损伤的作用。方法鼓膜穿刺术建立C57BL/6小鼠和IL-17A缺陷鼠急性中耳炎模型。收集中耳灌洗液,ELISA检测灌洗液中炎症因子和损伤标志物的表达。中耳组织石蜡切片经TUNEL染色和HE染色,观察小鼠中耳上皮细胞的凋亡和中耳组织损伤程度。采用广谱的凋亡抑制剂Z-VAD-FNK抑制凋亡后,观察中耳组织损伤的变化。结果 IL-17A显著上调白细胞介素6(IL-6)、肿瘤坏死因子α(TNF-α)和髓过氧化物酶(MPO)表达,加重了中耳炎症。IL-17A还促进了上皮细胞的凋亡和黏膜损伤。抑制凋亡后,显著降低了IL-17A介导的炎症反应,减轻了中耳组织损伤。结论 IL-17A可促进上皮细胞凋亡,加重中耳组织损伤。
Objective To establish a murine model of acute otitis media with Streptococcus pneumoniae and study the role of interleukin 17A (IL-17A) in promoting middle ear epithelial cell apoptosis and promoting middle ear injury. Methods The acute otitis media in C57BL / 6 mice and IL-17A-deficient mice were established by tympanotomy. Middle ear lavage fluid was collected and the expression of inflammatory cytokines and injury markers in lavage fluid was detected by ELISA. The paraffin sections of the middle ear were stained with TUNEL and HE staining to observe the apoptosis of the middle ear epithelium and the damage of middle ear tissue. A broad spectrum of apoptosis inhibitor Z-VAD-FNK was used to inhibit the apoptosis of the middle ear tissue. Results IL-17A significantly up-regulated the expression of interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α) and myeloperoxidase (MPO) IL-17A also promotes epithelial cell apoptosis and mucosal injury. Inhibition of apoptosis, significantly reduced the IL-17A-mediated inflammatory response, reduce the middle ear tissue injury. Conclusion IL-17A can promote epithelial cell apoptosis and aggravate the damage of middle ear tissue.