Lack of Effect of the Salmonella Deubiquitinase SseL on the NF-κB Pathway
Lack of Effect of the Salmonella Deubiquitinase SseL on the NF-κB Pathway
复制标题
沙门氏菌去泛素酶 SseL 对 NF-κB 通路缺乏影响
作者：
F. Mesquita;D. Holden;Nathalie Rolhion
肠道沙门氏菌的细胞内复制需要通过沙门氏菌致病岛-2（SPI-2）编码的III型分泌系统（T3 SS）跨含沙门氏菌的空泡膜转运效应蛋白。SPI-2 T3 SS效应子SseL是一种去泛素化酶，有助于小鼠的毒力。先前的工作已经产生了关于SseL参与干扰NF-κB通路的相互矛盾的证据。为了试图澄清这些差异，我们使用全基因组微阵列比较了野生型或sseL突变株感染的小鼠原代骨髓源性巨噬细胞的mRNA水平。SseL缺失对任何已知NF-κ B调控基因的mRNA水平均无可检测的影响。此外，SseL对（i）NF-κB通路的典型抑制剂（IκBα和磷酸化I κBα）和非典型NF-κB前体p100/p52的活化或水平，（ii）NF-κB转录因子p65向感染巨噬细胞核的易位和（iii）促炎细胞因子分泌无影响。此外，SseL的异位表达不影响报告细胞系中NF-κB的活化。这些结果不能支持SseL在宿主免疫应答的下调中的作用，特别是NF-κB途径。
Intracellular replication of Salmonella enterica requires effector proteins translocated across the Salmonella-containing vacuolar membrane by Salmonella pathogenicity island-2 (SPI-2) encoded type III secretion system (T3SS). The SPI-2 T3SS effector SseL is a deubiquitinase that contributes to virulence in mice. Previous work has produced conflicting evidence as to the involvement of SseL in interference with the NF-κB pathway. To attempt to clarify these discrepancies, we compared mRNA levels in mouse primary bone marrow-derived macrophages infected with wild-type or sseL mutant strains using a genome-wide microarray. There was no detectable effect of loss of SseL on mRNA levels corresponding to any known NF-κB-regulated gene. In addition, there was no effect of SseL on (i) the activation or levels of both the canonical inhibitor of the NF-κB pathway (IκBα and phospho-IκBα), and the non-canonical NF-κB precursor p100/p52, (ii) the translocation of the NF-κB transcription factor p65 to the nucleus of infected macrophages and (iii) pro-inflammatory cytokines secretion. Furthermore, ectopic expression of SseL did not affect NF-κB activation in reporter cell lines. These results fail to support a role for SseL in the down-regulation of the host immune response and in particular the NF-κB pathway.
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影响因子：
6
作者：
Ye, Zhongde;Petrof, Elaine O.;Sun, Jun
通讯作者：
Sun, Jun
影响因子：
16.8
作者：
Sun SC;Ley SC
通讯作者：
Ley SC
Yersinia YopJ 抑制 MAPK 和 NFkappaB 途径的体外信号传导。
影响因子：
--
作者：
Mukherjee,Sohini;Orth,Kim
通讯作者：
Orth,Kim
影响因子：
13
作者：
Basak, Soumen;Hoffmann, Alexander
通讯作者：
Hoffmann, Alexander
DOI：
10.1073/pnas.86.16.6383
发表时间：
1989-08-01
影响因子：
11.1
作者：
GALAN, JE;CURTISS, R
通讯作者：
CURTISS, R