严重脓毒症与免疫功能障碍  

Severe Sepsis and Immune Deficiency

作　　者：张庆红[1] 姚咏明[1] 

机构地区：[1]解放军总医院第一附属医院全军烧伤研究所,北京100048

出　　处：《医学与哲学（B）》2014年第1期18-22,27,共6页Medicine & Philosophy(B)

基　　金：国家自然科学基金资助项目;项目编号:81272089;81130035;81372054;81071545;国家重点基础研究发展计划项目;项目编号:2012CB518102;军队"十二五"医药卫生重点项目;项目编号:BWS12J050

摘　　要：脓毒症多呈现典型的促炎效应和抗炎反应,并与获得性免疫功能障碍同时出现,且免疫细胞中超过80%的基因表达发生改变。由于单核/巨噬细胞细胞因子谱的改变、主要组织相容性复合体Ⅱ类抗原(MHCⅡ)及共刺激分子表达下降以及树突状细胞的凋亡,诱发细胞免疫功能下降;中性粒细胞活性降低和补体系统的激活,又增加感染易感性。T淋巴细胞表现无反应性甚至凋亡,并向Th2漂移,同时免疫抑制性细胞功能增强,进一步发展则造成免疫麻痹,出现顽固性感染、器官衰竭甚至死亡。因此,阐明脓毒症免疫功能障碍的发病机制,进而明确机体的免疫状态,具有重要临床意义。Sepsis is a mixed inflammatory response, characterized by the occurrence of classical intlammarory anu anti- inflammatory, as well as adaptive immune response, with a global reprioritization affecting 〉80 % of the cellular functions and pathways. Due to the alterations of cytokine profile, and decreased expressions of MHC II and co-stimulating molecules on monocytes/macrophages, along with the apoptosis of dendritic cells, the cell-mediated immunity is significantly reduced. Moreover, the decreased neutrophil activity and complement activation result in the host more prone to infection. Attributed to the anergic and apoptotic T lymphoeytes, and the switch to Th2-1ike response of CD4＋ T cells, as well as the enhanced function of immune-suppressing cells, the immune function is severely impaired. Concomitant with the worsening of the above situations, the immune system is finally paralyzed, resulting recurrent infection, multiple organ failure, and even fatal outcome. Therefore, the elucidation of the mechanism for immune deficiency of sepsis, and identify the immunological status, is of critical importance.

关 键 词：脓毒症 危重症 代偿性抗炎反应综合征 免疫麻痹 医院获得性感染 

分 类 号：R826.3[医药卫生—临床医学]