Activation of the contact-phase system on bacterial surfaces -: a clue to serious complications in infectious diseases
Activation of the contact-phase system on bacterial surfaces -: a clue to serious complications in infectious diseases
复制标题
DOI：
10.1038/nm0398-298
复制
发表时间：
1998-03-01
期刊：
影响因子：
82.9
通讯作者：
Björck, L
中科院分区：
文献类型：
--
作者：
Herwald, H;Mörgelin, M;Björck, L
发烧、低血压和出血性疾病是败血症和感染性休克的常见症状。接触期系统的激活被认为通过触发促炎和促凝级联反应促进了这些严重疾病状态的发展；然而，潜在的分子机制尚不清楚。在这里，我们报道了接触相系统的组成部分通过它们与纤维性细菌表面蛋白、卷曲体和菌毛的特定相互作用组装在大肠杆菌和沙门氏菌表面。因此，促炎途径通过释放缓激肽而被激活，缓激肽是发烧、疼痛和低血压的有效诱导剂。细菌表面蛋白对接触期蛋白和纤维蛋白原的吸收会消耗相关凝血因子，导致低凝状态。因此，微生物表面蛋白和宿主接触期因子的复杂相互作用可能导致败血症和感染性休克的症状。
Fever, hypotension and bleeding disorders are common symptoms of sepsis and septic shock. The activation of the contact-phase system is thought to contribute to the development of these severe disease states by triggering proinflammatory and procoagulatory cascades; however, the underlying molecular mechanisms are obscure. Here we report that the components of the contact-phase system are assembled on the surface of Escherichia coli and Salmonella through their specific interactions with fibrous bacterial surface proteins, curli and fimbriae. As a consequence, the proinflammatory pathway is activated through the release of bradykinin, a potent inducer of fever, pain and hypotension. Absorption of contact-phase proteins and fibrinogen by bacterial surface proteins depletes relevant coagulation factors and causes a hypocoagulatory state. Thus, the complex interplay of microbe surface proteins and host contact-phase factors may contribute to the symptoms of sepsis and septic shock.