LPS介导的炎症反应过程及作用机制

被引：26

作者：

曹承华 ^{[1
]}

贺雅静 ^{[1
,2
]}

高荧苒 ^{[1
]}

施中东 ^{[1
]}

姬新颖 ^{[1
]}

机构：

[1] 河南大学医学院

[2] 商丘市第一人民医院

来源：

河南大学学报(医学版) | 2017年 / 36卷 / 01期

关键词：

LPS; 炎症反应; 作用机制;

D O I：

10.15991/j.cnki.41-1361/r.2017.01.020

中图分类号：

R364.5 [炎症];

学科分类号：

100104 ;

摘要：

LPS是革兰氏阴性菌的细胞壁主要组成成分,细菌死亡溶解或用人工方法破坏菌细胞后才释放出来。其毒性成分主要为类脂质A,能够引起哺乳动物细胞发生免疫反应,从而导致促炎因子的释放。通过细胞表面的先天免疫分子受体识别LPS是感染性休克的重要过程。严重感染,如肺炎、脓毒血症等是进入重症监护室的主要原因。LPS受体的识别、信号转导机制的研究是解决感染引起的炎症反应的重要环节,理解类脂A的生化修饰过程及其在发病机理过程中的作用可为这类疾病的治疗提供新的治疗方法。

引用

页码：70 / 76

页数：7

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