Trauma-hemorrhage and dendritic cell functions: a critical review of splenic dendritic cell dysfunction following trauma-hemorrhage and therapeutic approach
Trauma-hemorrhage and dendritic cell functions: a critical review of splenic dendritic cell dysfunction following trauma-hemorrhage and therapeutic approach
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DOI：
10.13172/2052-7853-1-2-979
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发表时间：
2013-09
期刊：
影响因子：
--
通讯作者：
T. Kawasaki;T. Sata
中科院分区：
文献类型：
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作者：
T. Kawasaki;T. Sata
创伤出血诱导的免疫抑制也与随后的脓毒症、器官衰竭和死亡率的易感性增加相关。以往的研究表明，创伤出血诱导先天免疫系统和适应性免疫系统的免疫抑制。腹腔、肺泡和脾巨噬细胞在创伤出血后释放白细胞介素（IL）-1、IL-6和肿瘤坏死因子（TNF）-α的能力在体外对脂多糖（LPS）刺激的反应中减弱。相比之下，枯否细胞已被证明具有增强的产生促炎性细胞因子的能力。
The trauma-hemorrhage- induced immunosuppression is also associated with an increased susceptibility to subsequent sepsis, organ failure and mortality. Previous studies demonstrated that trauma-hemorrhage induces immunosuppression in both innate immune systems and adaptive immune systems. The in vitro capacity of peritoneal, alveolar and splenic macrophages to release interleukin (IL)-1, IL-6 and tumour necrosis factor (TNF)-α in response to lipopolysaccharide (LPS) stimulation is diminished after traumahemorrhage. In contrast, Kupffer cells have been shown to have an enhanced capacity to produce pro-inflammatory