Holzmann B, Weighardt H, Heidecke C D
Chirurgische Klinik und Poliklinik,Technische Universität München, Munich.
Chirurg. 2003 Jan;74(1):61-4. doi: 10.1007/s00104-002-0592-4.
During polymicrobial sepsis,microbial pathogens and their products activate the innate immune system through signaling receptors of the Toll-like receptor (TLR) family, resulting in hyperinflammation and organ injury. The analysis of preclinical mouse models has shown that inactivation of the common TLR signaling adaptor protein MyD88 prevents the hyperinflammatory response and improves survival.Importantly, MyD88 deficiency does not impair antibacterial defense mechanisms.Thus,TLRs and proteins involved in TLR signaling may represent interesting targets for the development of new drugs for reprogramming pathophysiological immune responses during sepsis.
在多微生物败血症期间,微生物病原体及其产物通过Toll样受体(TLR)家族的信号受体激活先天免疫系统,导致过度炎症反应和器官损伤。临床前小鼠模型分析表明,常见的TLR信号衔接蛋白MyD88失活可防止过度炎症反应并提高生存率。重要的是,MyD88缺陷不会损害抗菌防御机制。因此,TLR及其信号传导相关蛋白可能是开发新型药物的有趣靶点,这些药物可在败血症期间重新编程病理生理免疫反应。