Sato K, Kawana M, Nonomura N, Nakano Y
Department of Otolaryngology, Niigata University School of Medicine, Japan.
Ann Otol Rhinol Laryngol. 1999 Jun;108(6):559-63. doi: 10.1177/000348949910800606.
To characterize the local response in acute otitis media, courses of interleukin (IL)-1beta, IL-6, IL-8, and tumor necrosis factor (TNF)alpha in middle ear fluid (MEF) of the guinea pig otitis media model induced by nonviable Haemophilus influenzae were investigated with enzyme-linked immunosorbent assay (ELISA) kits. The IL-1beta concentration in H. influenzae-inoculated ears peaked 24 hours after inoculation. The IL-8 concentration was significantly higher in H. influenzae-inoculated ears than in controls 48 and 96 hours after inoculation. The TNF-alpha concentration in H. influenzae-inoculated ears had an initial peak 6 hours after inoculation and had significant late increases 48 and 96 hours after inoculation. The results suggest that IL-1beta and TNF-alpha were produced by middle ear mucosa in the early stage of the experiment by stimulation of bacterial inoculation, which caused subsequent inflammatory cell accumulation, and that IL-8 and TNF-alpha were produced in the late stage by accumulating inflammatory cells.
为了描述急性中耳炎的局部反应,我们使用酶联免疫吸附测定(ELISA)试剂盒,对由非活性流感嗜血杆菌诱导的豚鼠中耳炎模型中耳积液(MEF)中的白细胞介素(IL)-1β、IL-6、IL-8和肿瘤坏死因子(TNF)α水平进行了研究。接种流感嗜血杆菌的耳朵中IL-1β浓度在接种后24小时达到峰值。接种流感嗜血杆菌的耳朵中IL-8浓度在接种后48小时和96小时显著高于对照组。接种流感嗜血杆菌的耳朵中TNF-α浓度在接种后6小时出现初始峰值,并在接种后48小时和96小时出现显著的后期升高。结果表明,在实验早期,IL-1β和TNF-α由中耳黏膜在细菌接种刺激下产生,这导致了随后的炎症细胞积聚;而IL-8和TNF-α在后期由积聚的炎症细胞产生。