Sips, Sops, and SPIs but not stn influence Salmonella enteropathogenesis.
Sips, Sops, and SPIs but not stn influence Salmonella enteropathogenesis.
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Sips、Sops 和 SPIs 但不影响沙门氏菌肠道发病机制。
DOI：
10.1007/978-1-4615-4143-1_29
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发表时间：
1999
影响因子：
--
通讯作者：
E. Galyov
中科院分区：
文献类型：
--
作者：
T. Wallis;M. Wood;P. Watson;S. Paulin;M. Jones;E. Galyov
影响沙门氏菌诱导的肠病发生的毒力因素的特征仍然很差。不同血清型沙门氏菌与牛回肠黏膜的相互作用已在结扎回肠环模型中被表征。在定量肠道入侵试验中，都柏林沙门氏菌、霍乱沙门氏菌、鸡产沙门氏菌和流产沙门氏菌菌株均从回肠黏膜中恢复，无论是否有Peyer斑块，数量相似。这一观察结果表明，肠道入侵的大小和途径并不介导沙门氏菌血清型宿主特异性。尽管具有相同的侵袭性，但这些血清型的肠致病性有明确的等级。肠致病性反应的大小与血清型宿主特异性无关。这些观察结果暗示了不确定的血清型特异性因素独立于肠道侵袭影响肠致病性。鼠伤寒沙门氏菌和都柏林沙门氏菌致病性岛（SPI） 1基因的破坏阻断了沙门菌入侵蛋白（Sips）和沙门菌外蛋白（Sops）的分泌。这些突变体在结扎回肠袢中的侵袭性和肠致病性明显低于野生型菌株。sopB和sopD的破坏可显著减少肠道发病，但不影响肠道侵袭。这两种基因似乎是协同作用的。令人惊讶的是，破坏stn（根据霍乱毒素同源性克隆的沙门氏菌肠毒素基因）并没有影响肠道发病。SopB被定位到鼠伤寒沙门氏菌的20厘米体上，其两侧有5个基因，它们以典型的致病性岛的方式组织，我们将其命名为SPI-5。SPI-5中其他基因的突变对小鼠的肠致病性也有减弱作用，但对小鼠的毒力没有减弱作用，提示SPI-5是特异性影响沙门氏菌肠致病性的关键基因座。
The virulence factors influencing Salmonella-induced enteropathogenesis remain poorly characterised. The interactions of different serotypes of Salmonella with bovine ileal mucosa have been characterised in the ligated ileal loop model. In a quantitative intestinal invasion assay Salmonella dublin, S. choleraesuis, S. gallinarum, and S. abortusovis strains were all recovered from ileal mucosa, either with or without Peyer's patches in similar numbers. This observation suggests that the magnitude and route of intestinal invasion does not mediate Salmonella serotype host specificity. Despite being equally invasive there was a clear hierarchy in the enteropathogenicity of these serotypes. The magnitude of the enteropathogenic responses did not correlate to serotype host specificity. These observations implicate undefined serotype specific factors in influencing enteropathogenicity independently of intestinal invasion. Disruption of genes in Salmonella Pathogenicity Island (SPI) 1 of S. typhimurium and S. dublin blocked the secretion of Salmonella Invasion Proteins (Sips) and Salmonella Outer Proteins (Sops). These mutants were significantly less invasive and enteropathogenic then the wild type strain in ligated ileal loops. Disruption of sopB and sopD significantly reduced enteropathogenesis, but without influencing intestinal invasion. These two genes appear to act in concert. Surprisingly, disruption of stn, the Salmonella enterotoxin gene cloned on the basis of its homology to cholera toxin, did not influence enteropathogenesis. SopB was mapped to the 20 centisome of S. typhimurium and is flanked by 5 genes that are organised in a manner typical of a pathogenicity island, which we have termed SPI-5. Mutation of the other genes in SPI-5 also attenuated enteropathogenesis but not virulence for mice, suggesting SPI-5 is a key locus specifically influencing Salmonella enteropathogenesis.