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目的:观察Clara细胞10-KDa蛋白(CC10)在小鼠细菌性慢性鼻-鼻窦炎(BCRS)模型中的表达。方法:C57BL/6J小鼠用鼻腔阻塞加肺炎链球菌接种的方法建立BCRS模型。用RT-PCR、免疫组织化学、组织病理染色及图像分析方法检测小鼠鼻窦黏膜组织CC10 mRNA及蛋白水平表达、CC10阳性细胞数及鼻窦黏膜形态学参数。结果:BCRS模型组小鼠鼻窦黏膜固有层内多型核中性粒细胞(PMN)数、上皮下胶原纤维沉积、上皮厚度及杯状细胞数均较假手术对照组增多(均P<0.01);BCRS组小鼠鼻窦黏膜上皮CC10阳性细胞数、CC10 mRNA及蛋白表达均较假手术对照组减少(均P<0.01)。CC10阳性细胞数分别与黏膜固有层PMN数、固有层胶原纤维沉积、上皮杯状细胞数及上皮厚度呈显著负相关,相关系数分别为-0.734、-0.776、-0.841和-0.805,均P<0.01;CC10平均灰度值分别与黏膜固有层PMN数、固有层胶原纤维沉积、上皮杯状细胞数及上皮厚度呈显著正相关,相关系数分别为0.771、0.802、0.887和0.855,均P<0.01。结论:小鼠BCRS模型鼻窦黏膜中CC10表达下调。CC10作为一种内源性负调控蛋白可能参与慢性鼻-鼻窦炎的发病过程。
OBJECTIVE: To observe the expression of 10-KDa protein (CC10) in Clara cells in bacterial chronic rhinosinusitis (BCRS) model in mice. Methods: BCRS model was established by intranasal occlusion plus S. pneumoniae inoculation in C57BL / 6J mice. The expression of CC10 mRNA and protein, the number of CC10 positive cells and the mucosal morphologic parameters of sinus mucosa were detected by RT-PCR, immunohistochemistry, histopathological staining and image analysis. Results: The numbers of polymorphonuclear neutrophil (PMN), sub-epithelial collagen fibers, epithelial thickness and number of goblet cells in the lamina propria of BCRS model group were significantly higher than those in sham operation group (all P <0.01) The number of CC10 positive cells and the expression of CC10 mRNA and protein in the mucosal epithelium of BCRS group were significantly lower than those in sham operation group (all P <0.01). The number of CC10 positive cells was negatively correlated with the number of PMN lamina propria, collagen deposition in lamina propria, goblet cells and epithelial thickness, the correlation coefficients were -0.734, -0.776, -0.841 and -0.805, respectively, P < 0.01 respectively. There was a significant positive correlation between the mean gray value of CC10 and the number of lamina propria PMN, the collagen deposition in lamina propria, the number of epithelial goblet cells and the thickness of epithelium, the correlation coefficients were 0.771,0.802,0.887 and 0.855, P <0.01 . Conclusion: The expression of CC10 in the mucosa of the BCRS mouse model is down-regulated. CC10 as an endogenous negative regulatory protein may be involved in the pathogenesis of chronic rhinosinusitis.