医学分子生物学杂志2012，Vol.9Issue(5)：439-442,4.DOI:10.3870/j.issn.1672-8009.2012.h5.027
Toll样受体4介导革兰阴性细菌的致病机制
Researches on Pathogenesis of Gram-Negative Bacteria Via Toll-Like Receptor 4
摘要
Abstract
Though it is well recognized that the immune response during Gram-negative bacterial infection is initiated after the recognition of endotoxin by Toll-like receptor 4 (TLR4) , the molecular mechanisms underling the inflammation response during Gram-negative bacterial infection remain poorly defined. Here, we show the studies which establish TLR4 as " master" regulator of in-flammasome activation by revealing the utilization of three signal pathways to orchestrate IL-1 β-driv-en inflammation. By engaging MyD88 downstream of TLR4, Gram-negative bacteria turn on transcription of pro- IL-1 β and of Nlrp3 mRNA ( signal 1 ) . Phagocytosis of bacteria and the destructive environment of the phagolysosomal compartment then lead to the release of bacteria] mRNA into the cytosolic compartment, allowing assembly of the NLRP3 inflammasome ( signal 2) . Engagement of TRIF downstream of TLR4 couples transcription of caspases-11 to its autoactivation via type I inter-feron ( signal 3) . Activated caspase-11 synergizes with the bacterial mRNA-assembled NLRP3 complex to coordinate caspase-1 activation and maturation of IL-l βand IL 18. These studies support the mechanism of TLR4 associated detrimental inflammation during Gram-negative bacterial infection.关键词
Toll样受体4/革兰阴性细菌/信号转导Key words
Toll-like receptor 4/ gram-negative bacteria/ signal transduction分类
医药卫生引用本文复制引用
许东,宋建新..Toll样受体4介导革兰阴性细菌的致病机制[J].医学分子生物学杂志,2012,9(5):439-442,4.
