大肠埃希菌脂多糖诱导的血小板降解及急性休克:O抗原在LPS诱导的免疫反应中的作用  

LPS from Escherichia coli induced platelet response and rapid shock in mice:contribution of O-antigen region of LPS in the immune reaction

作　　者：赵丽娟[1] 李文[2] 贺平 戚震伟[1] 陈春梅[1] 

机构地区：[1]大连大学附属医院口腔科,辽宁大连116022 [2]四川大学华西口腔医院 [3]大连市口腔医院

出　　处：《中国微生态学杂志》2006年第4期272-274,276,共4页Chinese Journal of Microecology

摘　　要：目的探讨LPS中的O抗原部分与其它部分在血小板反应中的作用。方法给BALB/c小鼠注入大肠埃希菌野生株E.coliO8、O9、K-12(不含有O抗原)及2株重组变异的K-12株(携带编码O8、O9的O抗原rfb基因)。结果K-12的LPS引起血小板反应及急性休克能力较弱,O8及O9引起一定的反应,而这2种重组的LPS,即在K-12的LPS上带有O8或O9的O抗原,显示出极强的活性。静脉注入补体C5的阻止剂后,重组株LPS的作用消失了。而且在缺乏补体C5小鼠DBA/2中,重组的LPS能引起血小板的聚集但不能降解,也不能引起休克症状。结论诱导血小板反应及急性休克的能力依赖于LPS结构;O抗原及R-核心抗原是表现活性的必要结构;LPS诱导的血小板反应及急性休克依赖补体系统。Objective To examine the contributions of O-antigen and the other components of LPS to the platelet response to LPS. Methods BALB/c mice were injected with the LPS from Eschreichia coli O8, O9 and K- 12 （without O-antigen）, and two from recombinant mutants of K-12 （with the gene coding O-antigen of 08 and 09 LPSs differently）, rOB, rO9. Results K-12 LPS had the weak ability to induce the platelet response or shock, and the ability of 08 and 09 LPS were common, while the 2 recombinant LPSs, rO8 and rOg, exhibited activities stronger than those of their original LPSs. Intravenous injection of the anticomplement agent made the ability of the platelet response and shock disappear, and so was in the DBA/2 mice. Conclusions The ability of inducing the platelet reaction and shock depend on the structure of LPS; O-antigen and R-core antigen were the important structure induced the platelet reaction and shock; and activation of the complement system was also involved in this response.

关 键 词：脂多糖 血小板反应 休克 

分 类 号：Q538[生物学—生物化学]