Gao Hongmei, Leaver Susannah K, Burke-Gaffney Anne, Finney Simon J
Unit of Critical Care Medicine, National Heart and Lung Institute, Imperial College, London, UK.
Semin Immunopathol. 2008 Feb;30(1):29-40. doi: 10.1007/s00281-007-0101-4. Epub 2007 Dec 11.
Severe sepsis dominates the mortality of non-cardiac intensive care units. The ingenious Toll-like receptor (TLR) system can recognise many infectious organisms through relatively few receptors to trigger pro-inflammatory and anti-inflammatory cytokine release. Further complexity arises from positive and negative signalling feedback loops. Severe sepsis may be a consequence of an inappropriately excessive response or inadequate endogenous negative feedback. Therapies targeting these pathways are currently being evaluated. Alternatively, in clinical scenarios such as compensatory anti-inflammatory response syndrome, chronic viral sepsis or inadequate vaccine function, TLR signalling may be inadequate. TLR agonists may augment the innate response and are being investigated.
严重脓毒症是非心脏重症监护病房死亡的主要原因。巧妙的Toll样受体（TLR）系统可以通过相对较少的受体识别多种感染性生物体，从而触发促炎和抗炎细胞因子的释放。正负信号反馈回路进一步增加了复杂性。严重脓毒症可能是反应过度不当或内源性负反馈不足的结果。目前正在评估针对这些途径的治疗方法。另外，在诸如代偿性抗炎反应综合征、慢性病毒性脓毒症或疫苗功能不足等临床情况下，TLR信号传导可能不足。TLR激动剂可能会增强先天反应，目前正在进行研究。
