Van Amersfoort Edwin S, Van Berkel Theo J C, Kuiper Johan
Division of Biopharmaceutics, Leiden/Amsterdam Center of Drug Research, Leiden University, Leiden, The Netherlands.
Clin Microbiol Rev. 2003 Jul;16(3):379-414. doi: 10.1128/CMR.16.3.379-414.2003.
Bacterial sepsis and septic shock result from the overproduction of inflammatory mediators as a consequence of the interaction of the immune system with bacteria and bacterial wall constituents in the body. Bacterial cell wall constituents such as lipopolysaccharide, peptidoglycans, and lipoteichoic acid are particularly responsible for the deleterious effects of bacteria. These constituents interact in the body with a large number of proteins and receptors, and this interaction determines the eventual inflammatory effect of the compounds. Within the circulation bacterial constituents interact with proteins such as plasma lipoproteins and lipopolysaccharide binding protein. The interaction of the bacterial constituents with receptors on the surface of mononuclear cells is mainly responsible for the induction of proinflammatory mediators by the bacterial constituents. The role of individual receptors such as the toll-like receptors and CD14 in the induction of proinflammatory cytokines and adhesion molecules is discussed in detail. In addition, the roles of a number of other receptors that bind bacterial compounds such as scavenger receptors and their modulating role in inflammation are described. Finally, the therapies for the treatment of bacterial sepsis and septic shock are discussed in relation to the action of the aforementioned receptors and proteins.
细菌败血症和脓毒性休克是由于免疫系统与体内细菌及细菌细胞壁成分相互作用，导致炎症介质过度产生所致。细菌细胞壁成分如脂多糖、肽聚糖和脂磷壁酸尤其应对细菌的有害作用负责。这些成分在体内与大量蛋白质和受体相互作用，这种相互作用决定了这些化合物最终的炎症效应。在循环系统中，细菌成分与诸如血浆脂蛋白和脂多糖结合蛋白等蛋白质相互作用。细菌成分与单核细胞表面受体的相互作用主要负责细菌成分诱导促炎介质。详细讨论了诸如Toll样受体和CD14等个别受体在促炎细胞因子和黏附分子诱导中的作用。此外，还描述了一些其他结合细菌化合物的受体的作用，如清道夫受体及其在炎症中的调节作用。最后，针对上述受体和蛋白质的作用，讨论了治疗细菌败血症和脓毒性休克的疗法。
