Wang Haichao, Zhu Shu, Zhou Rongrong, Li Wei, Sama Andrew E
Laboratory of Emergency Medicine, The Feinstein Institute for Medical Research, North Shore-LIJ Health System, Manhasset, NY 11030, USA.
Expert Rev Mol Med. 2008 Nov 4;10:e32. doi: 10.1017/S1462399408000884.
Sepsis refers to a systemic inflammatory response syndrome resulting from a microbial infection. The inflammatory response is partly mediated by innate immune cells (such as macrophages, monocytes and neutrophils), which not only ingest and eliminate invading pathogens but also initiate an inflammatory response upon recognition of pathogen-associated molecular patterns (PAMPs). The prevailing theories of sepsis as a dysregulated inflammatory response, as manifested by excessive release of inflammatory mediators such as tumour necrosis factor and high-mobility group box 1 protein (HMGB1), are supported by extensive studies employing animal models of sepsis. Here we review emerging evidence that support extracellular HMGB1 as a late mediator of experimental sepsis, and discuss the therapeutic potential of several HMGB1-targeting agents (including neutralising antibodies and steroid-like tanshinones) in experimental sepsis.
脓毒症是指由微生物感染引起的全身性炎症反应综合征。炎症反应部分由先天性免疫细胞(如巨噬细胞、单核细胞和中性粒细胞)介导,这些细胞不仅摄取和清除入侵的病原体,而且在识别病原体相关分子模式(PAMPs)后引发炎症反应。脓毒症作为一种炎症反应失调的流行理论,表现为肿瘤坏死因子和高迁移率族蛋白B1(HMGB1)等炎症介质的过度释放,这一理论得到了大量使用脓毒症动物模型的研究所支持。在此,我们综述了支持细胞外HMGB1作为实验性脓毒症晚期介质的新证据,并讨论了几种靶向HMGB1的药物(包括中和抗体和类甾体丹参酮)在实验性脓毒症中的治疗潜力。