Bansal Tarun, Jesudhasan Palmy, Pillai Suresh, Wood Thomas K, Jayaraman Arul
Artie McFerrin Department of Chemical Engineering, Texas A&M University, 222 Jack E. Brown Engineering Building, 3122 TAMU, College Station, TX 77843-3122, USA.
Appl Microbiol Biotechnol. 2008 Apr;78(5):811-9. doi: 10.1007/s00253-008-1359-8. Epub 2008 Feb 7.
The autoinducer-2 (AI-2) molecule is produced by many bacterial species, including various human gastrointestinal (GI) tract commensal bacteria, and has been proposed to be involved in interspecies communication. Because pathogens are likely to encounter AI-2 in the GI tract, we studied the effects of AI-2 on various phenotypes associated with enterohemorrhagic Escherichia coli (EHEC) infections. AI-2 attracted EHEC in agarose plug chemotaxis assays and also increased swimming motility, as well as increased EHEC attachment to HeLa cells. The molecular basis underlying the stimulation of EHEC chemotaxis, motility, and colonization by AI-2 was investigated at the transcriptome level using DNA microarrays. We found that exposure to AI-2 altered the expression of 23 locus of enterocyte effacement (LEE) genes directly involved in the production of virulence determinants, as well as other genes associated with virulence (e.g., 46 flagellar/fimbrial genes, 24 iron-related genes), in a temporally defined manner. To our knowledge, this is the first study to report AI-2-mediated regulation of EHEC chemotaxis and colonization, as well as temporal regulation of EHEC transcriptome by AI-2. Our results suggest that AI-2 is an important signal in EHEC infections of the human GI tract.
自诱导物-2(AI-2)分子由许多细菌种类产生,包括各种人类胃肠道共生菌,并被认为参与种间通讯。由于病原体可能在胃肠道中遇到AI-2,我们研究了AI-2对与肠出血性大肠杆菌(EHEC)感染相关的各种表型的影响。在琼脂糖栓趋化试验中,AI-2吸引了EHEC,还增加了其游动性,以及增加了EHEC对HeLa细胞的黏附。使用DNA微阵列在转录组水平研究了AI-2刺激EHEC趋化、运动和定殖的分子基础。我们发现,暴露于AI-2会以时间定义的方式改变23个肠上皮细胞损伤位点(LEE)基因的表达,这些基因直接参与毒力决定因素的产生,以及其他与毒力相关的基因(例如46个鞭毛/菌毛基因、24个铁相关基因)。据我们所知,这是第一项报道AI-2介导的EHEC趋化和定殖调节以及AI-2对EHEC转录组的时间调节的研究。我们的结果表明,AI-2是人类胃肠道EHEC感染中的一个重要信号。