LPS所介导的信号转导通路研究进展  

Progression of lipopolysaccharide signal pathway

作　　者：杨一新[1] 李桂源[1] 

机构地区：[1]中南大学肿瘤研究所,长沙410078

出　　处：《中南大学学报（医学版）》2006年第1期141-145,共5页Journal of Central South University ：Medical Science

基　　金：国家自然科学基金(30300205)

摘　　要：LPS是革兰氏阴性细菌的细胞壁主要组成成分,对LPS的识别与信号转导是机体自身防御反应的重要环节,同时也是导致内毒素性休克、全身炎症反应综合征和多器官功能衰竭等疾病的重要机制。LPS可通过LPS-LBP-sCD14三联复合物作用于TLR4并激活MyD88,活化的MyD88可聚集并结合IRAK1和IRAK2,然后作用于肿瘤坏死因子受体相关因子6(TRAF6),进一步激活MAPK和NF-κB信号转导通路。活化的MAPK和NF-κB信号转导通路是LPS所导致的细胞反应与炎症细胞因子如TNF-,αIL-6和IL-8等产生的重要分子机制。Lipopolysaccharide （ LPS ） is the major constituents of the outer membrane of Gramnegative bacteria. LPS recognition and signal transmission are key events in the host defense reaction towards Gram-negative bacteria and are associated with many disorders. Multiple signaling pathways are involved in the response to LPS. With the help of LPS-binding protein and CD14, TLR4 binds with LPS, then recruits myeloid differentiation factor 88 and IL-1 receptor-associated kinase, and further phosphorylates and activates TNF receptor associated factor 6 （ TRAF6 ）. The activated TRAF6 leads to the activation of transcription factor NF-κB and MAP kinase＇ s pathways that involves in LPS-induced cellular responses and the production of proinflammatory cytokines such as TNF-α, IL-6 and IL8.

关 键 词：LPS MAPK信号转导 NF-κB信号转导 

分 类 号：R363[医药卫生—病理学]