Host lipid sensing promotes invasion of cells with pathogenic Salmonella.
Host lipid sensing promotes invasion of cells with pathogenic Salmonella.
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DOI：
10.1038/s41598-018-33319-9
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发表时间：
2018-10-19
影响因子：
4.6
通讯作者：
Qadri A
中科院分区：
文献类型：
--
作者：
Shivcharan S;Yadav J;Qadri A
致病性沙门氏菌通过侵入非吞噬性肠上皮细胞（IEC）启动感染。这种入侵是由沙门氏菌致病岛-1（SPI-1）编码的许多沙门氏菌入侵促进分子（Sips）引起的。这些分子中的一些分子的细胞内递送也引起半胱天冬酶-1介导的有助于病原体清除的热凋亡细胞死亡。当沙门氏菌与一种或多种身份尚未确定的宿主信号接触时，这些分子被分泌并递送到细胞内。我们表明，溶血磷脂酰胆碱（LPC）释放后激活的半胱天冬酶-1在沙门氏菌感染的细胞和丰富的血浆放大生产的Sips从这种病原体，并促进其细胞入侵。LPC导致SipC的腺苷酸环化酶和cAMP受体蛋白（CRP）依赖性从头合成，伴随着其易位到细菌细胞表面并释放到外部环境中。用LPC处理沙门氏菌产生SPI - 1转录调节因子hilA的持续诱导。我们的发现揭示了一种新的宿主脂质传感驱动的沙门氏菌入侵调控机制。
Pathogenic Salmonella species initiate infection by invading non-phagocytic intestinal epithelial cells (IEC). This invasion is brought about by a number of Salmonella invasion promoting molecules (Sips) encoded by the Salmonella Pathogenicity Island - 1 (SPI-1). Intracellular delivery of some of these molecules also brings about caspase-1 – mediated pyroptotic cell death that contributes to pathogen clearance. These molecules are secreted and delivered inside cells upon contact of Salmonella with one or more host signals whose identity has not been established. We show that lysophosphatidylcholine (LPC) released following activation of caspase-1 in Salmonella – infected cells and abundant in plasma amplifies production of Sips from this pathogen and promotes its cellular invasion. LPC brings about adenylate cyclase and cAMP receptor protein (CRP) - dependent de novo synthesis of SipC that is accompanied by its translocation to bacterial cell surface and release into the outside milieu. Treatment of Salmonella with LPC produces sustained induction of SPI - 1 transcriptional regulator, hilA. Our findings reveal a novel host lipid sensing - driven regulatory mechanism for Salmonella invasion.
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