论文部分内容阅读
目的探讨表皮葡萄球菌(SE)感染引起新生小鼠脑损伤的机制。方法出生第1天新生小鼠共80只,分为SE组、生理盐水(NS)组、对照组,其中SE组48只,NS组及对照组各16只。SE组静脉注射108/ml的SE 50μl,NS组给予等量的NS,对照组不予任何处理。在注射后不同时间点(6 h、24 h、72 h、5 d、7 d)取血、脾、脑过夜培养后做细菌菌落(CFU)计数;在24 h和72 h取脑组织石蜡包埋后连续切片,用于离子钙接头蛋白抗体(Iba-1)免疫组化染色;在6 h和24 h取脑组织用酶联免疫吸附试验测定肿瘤坏死因子(TNF-α)、白介素-1β(IL-1β)、IL-5、IL-6。结果注射后不同时间点,SE组小鼠脑组织中均未发现细菌,血和脾中6 h菌落计数最高,24 h后迅速下降。在注射后24 h、72 h,SE组、NS组和对照组三组之间大脑中Iba-1阳性细胞数的差异有统计学意义(H=75.56、69.54,P均<0.001);其中SE组高于NS组和对照组,差异有统计学意义(P均<0.05)。各组在24 h与72 h两个时间点,大脑中Iba-1阳性细胞数差异无统计学意义(P均>0.05)。在注射后6 h、24 h,三组之间大脑TNF-α、IL-1β、IL-5和IL-6水平差异有统计学意义(H=59.07~319.34,P均<0.001);其中SE组大脑中各细胞因子含量均高于NS组和对照组,差异有统计学意义(P<0.05)。SE组在注射后24 h,与6 h时相比,TNF-α、IL-1β、IL-5和IL-6水平均有下降,两时间点差异均有统计学意义(P<0.01)。结论 SE引起的新生小鼠的脑损伤可能通过激活脑内小胶质细胞,同时分泌大量的细胞因子而引起。
Objective To investigate the mechanism of brain injury induced by Staphylococcus epidermidis (SE) in neonatal mice. Methods A total of 80 newborn mice were randomly divided into SE group, NS group and control group, including 48 in SE group, 16 in NS group and 16 in control group. In the SE group, SE 50μl was injected intravenously at a dose of 108 / ml. The NS group was given the same amount of NS, while the control group received no treatment. Bacterial colonies (CFU) were counted after culturing at different time points (6 h, 24 h, 72 h, 5 d, 7 d), and spleen and brain were cultured overnight. After 24 h and 72 h, Immunohistochemical staining of Iba-1 protein was performed on the surface of the brain tissue. Tumor necrosis factor (TNF-α), interleukin-1β (IL-1β), IL-5, IL-6. Results At different time points after injection, no bacteria were found in the brain of SE mice. The counts of 6 h colonies in blood and spleen were the highest at 24 h and then decreased rapidly. The numbers of Iba-1 positive cells in brain between SE group, NS group and control group were statistically significant at 24 h and 72 h after injection (H = 75.56, 69.54, P <0.001) Group higher than the NS group and the control group, the difference was statistically significant (P all <0.05). There was no significant difference in the number of Iba-1 positive cells in both groups at 24 h and 72 h (P> 0.05). The levels of TNF-α, IL-1β, IL-5 and IL-6 in the brain between the three groups were significantly different at 6 and 24 h after injection (H = 59.07 to 319.34, P <0.001) The contents of various cytokines in the brain of the group were higher than those of the NS group and the control group, with significant difference (P <0.05). The level of TNF-α, IL-1β, IL-5 and IL-6 decreased in SE group 24 h after injection compared with that at 6 h after injection. There was significant difference between two groups at the same time point (P <0.01). Conclusion The brain injury induced by SE in neonatal mice may be caused by the activation of microglia in the brain and the secretion of a large number of cytokines.