Hörner C, Bouchon A, Bierhaus A, Nawroth P P, Martin E, Bardenheuer H J, Weigand M A
Klinik für Anaesthesiologie, Universitätsklinikum Heidelberg, Germany.
Anaesthesist. 2004 Jan;53(1):10-28. doi: 10.1007/s00101-003-0626-4.
The innate immune system succeeds against the majority of infections before the adaptive immune system is activated. New findings contribute to a better understanding of the pathophysiology of sepsis and lead to the development of new therapeutic strategies. The innate immune system, being responsible for the first response to infections, can trigger adaptive immune responses in case the initial response is ineffective. Both arms of the immune system interact with each other, mainly via cell-cell-interactions but also by soluble factors, such as cytokines and chemokines. Two sub-populations of helper T-cells direct both balanced activation and inhibition of the two arms of the immune systems using specific patterns of cytokine release. Results obtained in new animal models of sepsis, taking a progressive growth of bacteria into account, have implied that existing knowledge has to be reanalyzed. The idea of sepsis as a mere "over-reaction to inflammation" has to be abandoned. Various so-called pattern recognition receptors (e.g. toll-like receptors, TLRs, NOD proteins) are located intracellularly or in the plasma membrane of innate immune cells and recognize certain patterns expressed exclusively by extracellular pathogens. Upon receptor engagement, intracellular signaling pathways lead to cellular activation, followed by release of various cytokines and anti-microbial substances. During the course of sepsis a cytokine shift towards increasing immune suppression occurs. The innate immune system also contributes to the migration of leukocytes in inflammed tissue, involving chemokines and adhesion molecules. Leukocytes also secrete the tissue factor leading to formation of thrombin. The environment in sepsis can cause disseminated intravascular coagulation (DIC), but at the same time thrombin triggers the release of chemokines and adhesion molecules through endothelial cells, which represents a positive feedback mechanism for innate immune responses. New therapeutic strategies for sepsis try to establish a well-balanced immune response. Intervention is accomplished through inhibition of inflammatory cytokines, their receptors or through activation of immunostimulatory responses.
在适应性免疫系统被激活之前,先天免疫系统就能成功抵御大多数感染。新的研究结果有助于更好地理解脓毒症的病理生理学,并推动新治疗策略的发展。先天免疫系统负责对感染的初始反应,若初始反应无效,它可触发适应性免疫反应。免疫系统的这两个分支相互作用,主要通过细胞间相互作用,也通过可溶性因子,如细胞因子和趋化因子。辅助性T细胞的两个亚群利用特定的细胞因子释放模式,直接调控免疫系统两个分支的平衡激活和抑制。在考虑细菌进行性生长的脓毒症新动物模型中获得的结果表明,现有知识必须重新分析。脓毒症仅仅是“对炎症的过度反应”这一观点必须摒弃。各种所谓的模式识别受体(如Toll样受体、TLRs、NOD蛋白)位于先天免疫细胞的细胞内或质膜中,识别仅由细胞外病原体表达的特定模式。受体结合后,细胞内信号通路导致细胞激活,随后释放各种细胞因子和抗菌物质。在脓毒症过程中,会出现细胞因子向免疫抑制增加的转变。先天免疫系统也有助于白细胞在炎症组织中的迁移,涉及趋化因子和黏附分子。白细胞还分泌组织因子导致凝血酶形成。脓毒症环境可导致弥散性血管内凝血(DIC),但同时凝血酶通过内皮细胞触发趋化因子和黏附分子的释放,这代表了先天免疫反应的一种正反馈机制。脓毒症的新治疗策略试图建立一种平衡良好的免疫反应。干预通过抑制炎性细胞因子、其受体或通过激活免疫刺激反应来实现。