A secreted effector protein of Salmonella dublin is translocated into eukaryotic cells and mediates inflammation and fluid secretion in infected ileal mucosa
A secreted effector protein of Salmonella dublin is translocated into eukaryotic cells and mediates inflammation and fluid secretion in infected ileal mucosa
复制标题
DOI：
10.1111/j.1365-2958.1997.mmi525.x
复制
发表时间：
1997-09-01
影响因子：
3.6
通讯作者：
Wallis, TS
中科院分区：
文献类型：
--
作者：
Galyov, EE;Wood, MW;Wallis, TS
由非伤寒致病性沙门氏菌引起的肠炎的特征在于受感染回肠中的液体分泌和炎症反应。沙门氏菌引起的炎症反应最初主要由中性粒细胞（PMN）迁移到肠粘膜和肠腔组成。沙门氏菌和肠上皮细胞之间的相互作用在诱导炎症反应中起着重要作用。在与上皮细胞相互作用后，鲑鱼精能够引起向中性粒细胞的跨上皮信号传导。这种信号传导被认为是沙门氏菌诱导的肠炎的关键毒力特征。然而，这种信号的性质和机制迄今尚未澄清。在这里，我们的特点SopB，一种新的分泌的效应蛋白的都柏林沙门氏菌，目前的数据表明，SopB易位到真核细胞通过一个SIP依赖的途径，以促进液体分泌和炎症反应在感染的回肠。
Enteritis induced by non-typhoid pathogenic Salmonella is characterized by fluid secretion and inflammatory responses in the infected ileum. The inflammatory response provoked by Salmonella initially consists largely of a neutrophil (PMN) migration into the intestinal mucosa and the gut lumen. The interactions between Salmonella and intestinal epithelial cells are known to play an essential role in inducing the inflammatory response. Upon interaction with epithelial cells salmonellae are able to elicit transepithelial signalling to neutrophils. This signalling is recognized as a key virulence feature underlying Salmonella-induced enteritis. However, the nature and mechanism of such signalling has not been clarified to date. Here, we characterize SopB, a novel secreted effector protein of Salmonella dublin, and present data implying that SopB is translocated into eukaryotic cells via a sip-dependent pathway to promote fluid secretion and inflammatory responses in the infected ileum.