Perrett Charlotte A, Karavolos Michail H, Humphrey Suzanne, Mastroeni Pietro, Martinez-Argudo Isabel, Spencer Hannah, Bulmer David, Winzer Klaus, McGhie Emma, Koronakis Vassilis, Williams Paul, Khan C M Anjam, Jepson Mark A
Department of Biochemistry, School of Medical Sciences, University of Bristol, Bristol, United Kingdom.
J Bacteriol. 2009 Dec;191(23):7253-9. doi: 10.1128/JB.00727-09. Epub 2009 Sep 25.
Bacterial species can communicate by producing and sensing small autoinducer molecules by a process known as quorum sensing. Salmonella enterica produces autoinducer 2 (AI-2) via the luxS synthase gene, which is used by some bacterial pathogens to coordinate virulence gene expression with population density. We investigated whether the luxS gene might affect the ability of Salmonella enterica serovar Typhimurium to invade epithelial cells. No differences were found between the wild-type strain of S. Typhimurium, SL1344, and its isogenic luxS mutant with respect to the number and morphology of the membrane ruffles induced or their ability to invade epithelial cells. The dynamics of the ruffling process were also similar in the wild-type strain (SL1344) and the luxS mutant. Furthermore, comparing the Salmonella pathogenicity island 1 (SPI-1) type 3 secretion profiles of wild-type SL1344 and the luxS mutant by Western blotting and measuring the expression of a single-copy green fluorescent protein fusion to the prgH (an essential SPI-1 gene) promoter indicated that SPI-1 expression and activity are similar in the wild-type SL1344 and luxS mutant. Genetic deletion of luxS did not alter the virulence of S. Typhimurium in the mouse model, and therefore, it appears that luxS does not play a significant role in regulating invasion of Salmonella in vitro or in vivo.
细菌物种可以通过一种称为群体感应的过程产生并感知小的自诱导分子来进行通讯。肠炎沙门氏菌通过luxS合酶基因产生自诱导物2（AI-2），一些细菌病原体利用它来根据种群密度协调毒力基因的表达。我们研究了luxS基因是否可能影响鼠伤寒沙门氏菌肠炎血清型侵袭上皮细胞的能力。在鼠伤寒沙门氏菌野生型菌株SL1344及其同基因luxS突变体之间，在诱导的膜皱褶数量和形态或其侵袭上皮细胞的能力方面未发现差异。野生型菌株（SL1344）和luxS突变体中皱褶过程的动力学也相似。此外，通过蛋白质免疫印迹比较野生型SL1344和luxS突变体的沙门氏菌致病岛1（SPI-1）3型分泌谱，并测量与prgH（一个必需的SPI-1基因）启动子融合的单拷贝绿色荧光蛋白的表达，表明野生型SL1344和luxS突变体中SPI-1的表达和活性相似。luxS的基因缺失并未改变鼠伤寒沙门氏菌在小鼠模型中的毒力，因此，似乎luxS在体外或体内调节沙门氏菌的侵袭中不发挥重要作用。
