Osada Rika, Takeno Sachio, Hirakawa Katsuhiro, Ueda Tsutomu, Furukido Kyosuke, Yajin Koji
Department of Otolaryngology, Hiroshima University School of Medicine, Kasumi 1-2-3, Minami-ku, Hiroshima 734-8551, Japan.
Rhinology. 2003 Jun;41(2):80-6.
The purpose of this study was to compare the expression of cytokines and nuclear factor-kappa B (NF-kappa B) subunits in cultured sinus mucosal cells by semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) in chronic sinusitis patients with allergic rhinitis (abbreviated as AR patients) versus patients without AR (abbreviated as non-AR patients). The localization of p50 in cultured sinus mucosal cells was also observed by immunocytochemistry. The expression of messenger RNAs (mRNA) encoding granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin (IL)-6, IL-8, p50 and p65 subunits, and inhibitory kappa B-alpha (I kappa B-alpha) were analyzed by RT-PCR. The proportion of active NF-kappa B-positive cells in the epithelial layer was analyzed using a laser-scanning confocal microscope image system. The levels of GM-CSF, IL-6, IL-8, and p50 mRNAs in AR patients were significantly higher than those in non-AR patients (p < 0.01, p < 0.01, p < 0.01, and p < 0.001, respectively). Immunocytochemical reaction for p50 in sinus mucosal cells in AR patients showed more intense nuclear staining compared to non-AR patients. These findings could support the hypothesis that the increase of cytokines from sinus mucosal cells in AR patients was associated with augmented NF-kappa B mRNA expression, resulting in the modification of the cytokine network.
本研究旨在通过半定量逆转录-聚合酶链反应(RT-PCR)比较变应性鼻炎慢性鼻窦炎患者(简称为AR患者)与无变应性鼻炎患者(简称为非AR患者)培养的鼻窦黏膜细胞中细胞因子和核因子-κB(NF-κB)亚基的表达。还通过免疫细胞化学观察了p50在培养的鼻窦黏膜细胞中的定位。通过RT-PCR分析编码粒细胞-巨噬细胞集落刺激因子(GM-CSF)、白细胞介素(IL)-6、IL-8、p50和p65亚基以及抑制性κB-α(IκB-α)的信使核糖核酸(mRNA)的表达。使用激光扫描共聚焦显微镜图像系统分析上皮层中活性NF-κB阳性细胞的比例。AR患者中GM-CSF、IL-6、IL-8和p50 mRNA的水平显著高于非AR患者(分别为p<0.01、p<0.01、p<0.01和p<0.001)。与非AR患者相比,AR患者鼻窦黏膜细胞中p50的免疫细胞化学反应显示核染色更强。这些发现可能支持以下假设:AR患者鼻窦黏膜细胞中细胞因子的增加与NF-κB mRNA表达增强有关,从而导致细胞因子网络的改变。