华支睾吸虫感染对大鼠肠道菌群移位和内毒素血症的影响

目的研究肠道细菌移位在华支睾吸虫病致病机制中的作用。方法建立华支睾吸虫感染大鼠模型。分别在造模后48 h(后尾蚴期)、18 d(童虫期)和35 d(成虫期),取肝、肺、淋巴结和血液组织,采用平板培养法进行细菌移位的检测;采用鲎三肽基质染色定量法检测血浆内毒素含量。结果感染18 d后,实验组肠道细菌移位率开始增高,至感染35 d时,细菌移位率为70%,明显高于对照组的10%,差异有统计学意义(P=0.0230.05);感染鼠以童虫期、成虫期细菌移位现象明显,总移位率为65%,与对照组10%比较,差异有统计学意义(u=3.59,P0.01),且在肝、肺、淋巴结和血液组织中,移位发生率分别为60%、15%、25%和10%,以肝脏部位最高;造模后18 d血浆内毒素水平明显增高,造模后35 d血浆LPS水平略有下降,但仍明显高于对照组,差异有统计学意义(t=7.612,P0.01)。结论华支睾吸虫感染可引发宿主肠道菌群移位,以肝组织多发,从而参与致病机制。

The influence of Clonorchis sinensis infection on intestinal bacteria translocation and endotoxemia of rat

Abstract: Objective To study the role of intestinal bacterial translocation in Clonorchis sinensis pathogenic mechanism. Methods The rat model of Clonorchis sinensis infection was established. After 48 h (larvae), 18 d (child), 35 d (adult), taking liver, lung, lymph node and blood tissue to detect bacterial translocation and the endotoxin content in plasma by using plate culture method and limulus tripeptide matrix dyeing quantitative method respectively. Results After infecting 18 d, the intestinal bacterial translocation rate of the experimental group began to rise. When infecting 35 d, the bacterial translocation rate was 70%, significantly higher than the control group (10%, P<0.05). Bacterial translocation phenomenon was obvious in infected rats during their child and adult stage, with a total translocation rate of 65%. Compared with the control group (10%), difference was extremely significant (P<0.01). In liver, lung, lymph node and blood tissue, the translocation rate were 60%, 15%, 25% and 10% respectively, with liver showing the highest rate. After establishing the model for 18 d, the endotoxin content in plasma increased significantly (P<0.01). After establishing the model for 35 d, plasma LPS level showed a slight decline, but still significantly higher than that of the control group (P<0.01). Conclusion Clonorchis sinensis infection can cause host intestinal bacterial translocation and most often occur in liver tissue, thereby participating in pathogenic mechanism.