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Salmonella enterica Serovar Typhimurium Invasion Is Repressed in the Presence of Bile

机译：胆汁中抑制沙门氏菌血清型鼠伤寒沙门氏菌入侵。

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As enteric pathogens, the salmonellae have developed systems by which they can sense and adapt appropriately to deleterious intestinal components that include bile. Previously, growth in the presence of bile was shown to repress the transcription of prgH, a locus encoding components of the Salmonella pathogenicity island I (SPI-1) type III secretion system (TTSS) necessary for eukaryotic cell invasion. This result suggested an existing interaction between salmonellae, bile, and eukaryotic cell invasion. Transcription assays demonstrated that invasion gene regulators (e.g.,sirC and invF) are repressed by bile. However, bile does not interact with any of the invasion regulators directly but exerts its effect at or upstream of the two-component system at the apex of the invasion cascade, SirA-BarA. As suggested by the repression of invasion gene transcription in the presence of bile, Western blot analysis demonstrated that proteins secreted by the SPI-1 TTSS were markedly reduced in the presence of bile. Furthermore, Salmonella enterica serovar Typhimurium grown in the presence of bile was able to invade epithelial cells at only 4% of the level of serovar Typhimurium grown without bile. From these data, we propose a model whereby serovar Typhimurium uses bile as an environmental signal to repress its invasive capacity in the lumen of the intestine, but upon mucous layer penetration and association with intestinal epithelial cells, where the apparent bile concentration would be reduced, the system would become derepressed and invasion would be initiated.
机译：沙门氏菌是肠道病原体，已开发出各种系统，通过它们可以感应并适当适应包括胆汁在内的有害肠道成分。以前，在胆汁存在下生长显示抑制 prgH 的转录，prgH 是编码沙门氏菌致病岛I（SPI-1）III型分泌系统的基因座。 （TTSS）是真核细胞入侵所必需的。该结果表明沙门氏菌，胆汁和真核细胞入侵之间存在相互作用。转录分析表明，入侵基因调节剂（例如， sirC 和 invF ）被胆汁抑制。但是，胆汁不会直接与任何入侵调节因子发生相互作用，而是会在入侵级联顶点SirA-BarA的两组分系统或其上游发挥作用。正如在胆汁存在下抑制入侵基因转录所表明的那样，蛋白质印迹分析表明，在胆汁存在下，由SPI-1 TTSS分泌的蛋白质明显减少。此外，在胆汁中生长的 Salmonella enterica 鼠伤寒血清能够入侵上皮细胞，其水平仅为无胆汁鼠伤寒血清的4％。根据这些数据，我们提出了一个模型，其中鼠伤寒血清利用胆汁作为环境信号来抑制其在肠腔中的侵袭能力，但是在粘液层渗透并与肠道上皮细胞结合后，表观胆汁浓度会降低，该系统将被取消压制并开始入侵。

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