Wallis T S, Galyov E E
Institute for Animal Health, Compton, Berkshire RG20 7NN, UK.
Mol Microbiol. 2000 Jun;36(5):997-1005. doi: 10.1046/j.1365-2958.2000.01892.x.
Salmonella pathogenesis is a complex and multifactorial phenomenon. Many genes required for full virulence in mice have been identified, but only a few of these have been shown to be necessary for the induction of enteritis. Likewise, at least some of the Salmonella virulence factors affecting enteritis do not appear to be required for infection of systemic sites in mice. This suggests that subsets of virulence genes influence distinct aspects of Salmonella pathogenesis. Recently, considerable progress has been made in characterizing the virulence mechanisms influencing enteritis caused by non-typhoid Salmonella spp. The Salmonella pathogenicity island-1-encoded type III secretion system mediates the translocation of secreted effector proteins into target epithelial cells. These effector proteins are key virulence factors required for Salmonella intestinal invasion and the induction of fluid secretion and inflammatory responses.
沙门氏菌发病机制是一个复杂的多因素现象。已鉴定出许多在小鼠中实现完全毒力所需的基因,但其中只有少数被证明是诱发肠炎所必需的。同样,至少一些影响肠炎的沙门氏菌毒力因子似乎并非小鼠全身性感染所必需。这表明毒力基因亚群影响沙门氏菌发病机制的不同方面。最近,在表征影响非伤寒沙门氏菌引起的肠炎的毒力机制方面取得了相当大的进展。沙门氏菌致病岛1编码的III型分泌系统介导分泌的效应蛋白转运到靶上皮细胞中。这些效应蛋白是沙门氏菌肠道侵袭以及诱导液体分泌和炎症反应所需的关键毒力因子。