Inflammatory cAMP signaling and cell migration genes co-opted by the anthrax bacillus
Inflammatory cAMP signaling and cell migration genes co-opted by the anthrax bacillus
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DOI：
10.1073/pnas.0800105105
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发表时间：
2008-04-22
影响因子：
11.1
通讯作者：
Park, Jin Mo
中科院分区：
文献类型：
--
作者：
Kim, Chun;Wilcox-Adelman, Sarah;Park, Jin Mo
炭疽杆菌是炭疽病的病原体，它避开了免疫监视，并征用宿主巨噬细胞作为淋巴扩散的媒介。在这里，我们证明了B。炭疽水肿毒素（ET）通过其腺苷酸环化酶活性显著增加感染的巨噬细胞的运动性和血管内皮生长因子的表达。转录因子CREB和syndecan-1基因（CREB靶基因）在ET诱导的巨噬细胞迁移中起关键作用。这些分子和细胞反应发生在巨噬细胞中，巨噬细胞参与了β-CD G蛋白偶联受体的活化，从而说明了一个共同的信号传导回路，控制炎症的解决和宿主细胞被B劫持。炭疽病
Bacillus anthracis, the etiologic agent of anthrax, avoids immune surveillance and commandeers host macrophages as a vehicle for lymphatic spreading. Here, we show that B. anthracis edema toxin (ET), via its adenylyl cyclase activity, dramatically increases the motility of infected macrophages and the expression of vascular endothelial growth factor. The transcription factor CREB and the syndecan-1 gene, a CREB target, play crucial roles in ET-induced macrophage migration. These molecular and cellular responses occur in macrophages engaged in antiinflammatory G protein-coupled receptor activation, thus illustrating a common signaling circuitry controlling resolution of inflammation and host cell hijacking by B. anthracis.