Mechanisms involved in the adaptation of Escherichia coli O157:H7 to the host intestinal microenvironment.
Mechanisms involved in the adaptation of Escherichia coli O157:H7 to the host intestinal microenvironment.
复制标题
DOI：
10.1042/cs20200971
复制
发表时间：
2020-12
期刊：
影响因子：
6
通讯作者：
R. Fernandez-Brando;S. McAteer;Johanna Montañez-Culma;Y. Cortés-Araya;J. Tree;A. Bernal;Federico Fuentes;Stephen F. Fitzgerald;G. Pineda;M. V. Ramos;D. Gally;M. Palermo
中科院分区：
文献类型：
--
作者：
R. Fernandez-Brando;S. McAteer;Johanna Montañez-Culma;Y. Cortés-Araya;J. Tree;A. Bernal;Federico Fuentes;Stephen F. Fitzgerald;G. Pineda;M. V. Ramos;D. Gally;M. Palermo
病原体的宿主适应性可能增加种内和种间传播。我们以前表明，临床分离的肠出血性大肠杆菌（EHEC）O 157菌株（125/99）通过小鼠胃肠道的通道增加了其在同一宿主中的致病性。在这项工作中，我们的目的是阐明粪便回收（125 RR）菌株的病理适应的潜在机制。我们利用基因芯片技术对125/99株和125/99株的基因表达谱进行了分析，发现125/99株和125/99株有近100个基因表达差异。我们在mRNA和蛋白质水平检测到三型分泌系统（TTSS）蛋白的过表达，并证明125 RR株与上皮细胞系的粘附增加。125 RR菌株的其他关键属性是：在半固体琼脂上的运动性增加，这与fliC mRNA水平增加相关;在mRNA和蛋白质水平上减少Stx 2的产生;在pH 2.5下的存活率增加，如通过耐酸性测定所确定的。我们测试了在125/99菌株中LEE编码的调节子（ler）的反式过表达是否可以重现在125 RR菌株中观察到的致病性增加。如预期的，ler过表达导致TTSS蛋白表达增加和细菌粘附到体外上皮细胞，但也增加了体内死亡率和肠定植。我们的结论是，这个主机适应过程中需要的几个机制，提高肠出血性大肠杆菌O 157健身在新的主机的变化。这项研究强调了这些人畜共患病病原体在动物和人类之间水平传播所需的一些细菌机制。
Host adaptation of pathogens may increase intra- and interspecies transmission. We showed previously that the passage of a clinically isolated enterohemorrhagic Escherichia coli (EHEC) O157 strain (125/99) through the gastrointestinal tract of mice increases its pathogenicity in the same host. In this work, we aimed to elucidate the underlying mechanism(s) involved in the patho-adaptation of the stool-recovered (125RR) strain. We assessed the global transcription profile by microarray and found almost 100 differentially expressed genes in 125RR strain compared with 125/99 strain. We detected an overexpression of Type Three Secretion System (TTSS) proteins at the mRNA and protein levels and demonstrated increased adhesion to epithelial cell lines for the 125RR strain. Additional key attributes of the 125RR strain were: increased motility on semisolid agar, which correlated with an increased fliC mRNA level; reduced Stx2 production at the mRNA and protein levels; increased survival at pH 2.5, as determined by acid resistance assays. We tested whether the overexpression of the LEE-encoded regulator (ler) in trans in the 125/99 strain could recreate the increased pathogenicity observed in the 125RR strain. As anticipated ler overexpression led to increased expression of TTSS proteins and bacterial adhesion to epithelial cells in vitro but also increased mortality and intestinal colonization in vivo. We conclude that this host-adaptation process required changes in several mechanisms that improved EHEC O157 fitness in the new host. The research highlights some of the bacterial mechanisms required for horizontal transmission of these zoonotic pathogens between their animal and human populations.