Division of Biomedical Food Research, National Institute of Health Sciences, Kamiyoga 1-18-1, Setagaya-ku, Tokyo 158-8501, Japan.
Biochem Biophys Res Commun. 2012 Oct 5;426(4):654-8. doi: 10.1016/j.bbrc.2012.09.012. Epub 2012 Sep 10.
Salmonella enterica serovar Typhimurium is a major cause of human gastrointestinal illness worldwide. This pathogen can persist in a wide range of environments, making it of great concern to public health. Here, we report that the salmonella pathogenicity island (SPI)-1 effector protein SipB exhibits a membrane topology that confers bacterial osmotolerance. Disruption of the sipB gene or the invG gene (SPI-1 component) significantly reduced the osmotolerance of S. Typhimurium LT2. Biochemical assays showed that NaCl osmolarity increased the membrane topology of SipB, and a neutralising antibody against SipB reduced osmotolerance in the WT strain. The WT strain, but not the sipB mutant, exhibited elevated cyclopropane fatty acid C19:0 during conditions of osmotic stress, correlating with the observed levels of survival and membrane integrity. This result suggests a link between SipB and the altered fatty acid composition induced upon exposure to osmotic stress. Overall, our findings provide the first evidence that the Salmonella virulence translocon SipB affects membrane fluidity and alters bacterial osmotolerance.
鼠伤寒沙门氏菌是一种全球性的人类胃肠道疾病的主要原因。这种病原体可以在广泛的环境中存活，因此对公共健康构成了极大的威胁。在这里，我们报告称，沙门氏菌致病性岛（SPI）-1效应蛋白 SipB 表现出一种赋予细菌耐渗透压的膜拓扑结构。sipB 基因或 invG 基因（SPI-1 成分）的破坏显著降低了鼠伤寒沙门氏菌 LT2 的耐渗透压性。生化分析表明，NaCl 渗透压增加了 SipB 的膜拓扑结构，针对 SipB 的中和抗体降低了 WT 菌株的耐渗透压性。WT 菌株，但不是 sipB 突变体，在渗透压应激条件下表现出升高的环丙烷脂肪酸 C19:0，与观察到的存活和膜完整性水平相关。这一结果表明 SipB 与暴露于渗透压应激时诱导的脂肪酸组成的改变之间存在联系。总的来说，我们的研究结果首次提供了证据表明，沙门氏菌毒力转位体 SipB 影响膜流动性并改变细菌的耐渗透压性。
