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都柏林沙门氏菌分泌的效应蛋白SopA被转运到真核细胞中,并影响肠炎的诱导。

The secreted effector protein of Salmonella dublin, SopA, is translocated into eukaryotic cells and influences the induction of enteritis.

作者信息

Wood M W, Jones M A, Watson P R, Siber A M, McCormick B A, Hedges S, Rosqvist R, Wallis T S, Galyov E E

机构信息

Institute for Animal Health, Compton, Berkshire, UK.

出版信息

Cell Microbiol. 2000 Aug;2(4):293-303. doi: 10.1046/j.1462-5822.2000.00054.x.

Abstract

Salmonella-induced enteritis is associated with the induction of an acute intestinal inflammatory response and net fluid secretion into the lumen of infected mucosa. Proteins secreted by the Inv/Spa type III secretion system of Salmonella play a key role in the induction of these responses. We have demonstrated recently that the Inv/Spa-secreted SopB and SopD effector proteins are translocated into eukaryotic cells via a Sip-dependent pathway and act in concert to mediate inflammation and fluid secretion in infected ileal mucosa. Mutations of both sopB and sopD significantly reduced, but did not abrogate, the enteropathogenic phenotype. This indicated that other virulence factors are involved in the induction of enteritis. In this work, we characterize SopA, a secreted protein belonging to the family of Sop effectors of Salmonella dublin. We demonstrate that SopA is translocated into eukaryotic cells and provide evidence suggesting that SopA has a role in the induction of enteritis.

摘要

沙门氏菌引起的肠炎与急性肠道炎症反应的诱导以及感染黏膜腔中的净液体分泌有关。沙门氏菌的Inv/Spa III型分泌系统分泌的蛋白质在这些反应的诱导中起关键作用。我们最近证明,Inv/Spa分泌的SopB和SopD效应蛋白通过依赖Sip的途径转运到真核细胞中,并协同作用介导感染回肠黏膜中的炎症和液体分泌。sopB和sopD的突变均显著降低但并未消除肠道致病表型。这表明其他毒力因子也参与肠炎的诱导。在这项工作中,我们对SopA进行了表征,SopA是一种属于都柏林沙门氏菌Sop效应蛋白家族的分泌蛋白。我们证明SopA可转运到真核细胞中,并提供证据表明SopA在肠炎的诱导中起作用。

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