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首页> 外文期刊>Journal of endotoxin research >Deacylation and palmitoylation of lipid A by Salmonellae outer membrane enzymes modulate host signaling through Toll-like receptor 4.
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Deacylation and palmitoylation of lipid A by Salmonellae outer membrane enzymes modulate host signaling through Toll-like receptor 4.

机译:沙门氏菌外膜酶对脂质A的去酰化和棕榈酰化通过Toll样受体4调节宿主信号传导。

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摘要

The Salmonella typhimurium virulence gene products, PhoP/PhoQ sense host micro-environments to regulate the expression of a lipid A 3-O-deacylase, PagL, and a lipid A palmitoyltransferase, PagP. Therefore, deacylation and/or palmitoylation of lipid A could occur in Salmonellae adapted to host environments. The acylation state of lipid A can alter host recognition and signaling by Toll-like receptor (TLR) 4, and may play an important role in host defenses against Salmonellae infection. Deacylated lipid A, deacylated and palmitoylated lipid A, palmitoylated lipid A, and unmodified lipid A species were purified, and the activity was examined using cell lines expressing recombinant human or mouse TLR4. Compared with unmodified lipid A, the modified lipid A species are 10-100-fold less active. These results suggest that PagL and PagP modify lipid A to reduce TLR4-signaling as part of Salmonellae adaptation to the host environment.
机译:鼠伤寒沙门氏菌毒力基因产品PhoP / PhoQ有义宿主可调控微环境,以调节脂质A 3-O-脱酰基酶PagL和脂质A棕榈酰转移酶PagP的表达。因此,在适应宿主环境的沙门氏菌中可能发生脂质A的去酰化和/或棕榈酰化。脂质A的酰化状态可以通过Toll样受体(TLR)4改变宿主的识别和信号传导,并且可能在宿主防御沙门氏菌感染中发挥重要作用。纯化去酰基化的脂质A,去酰基化的和棕榈酰化的脂质A,棕榈酰化的脂质A和未修饰的脂质A物质,并使用表达重组人或小鼠TLR4的细胞系检查活性。与未修饰的脂质A相比,修饰的脂质A的活性低10-100倍。这些结果表明,PagL和PagP修饰脂质A以减少作为沙门氏菌适应宿主环境的一部分的TLR4信号传导。

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