CexE is a 12 kDa protein that was originally reported to be present in just three strains of enterotoxigenic Escherichia coli (ETEC); a frequent cause of diarrheal illnesses worldwide. However, an examination of sequenced genomes has revealed that CexE is actually present in a majority of ETEC strains. In addition, homologs of CexE are present in enteroaggregative E. coli (EAEC), Yersinia enterocolitica, Providencia alcalifaciens, and Citrobacter rodentium. Although it has been hypothesized that CexE and its homologs are virulence factors, this has yet to be tested. Thus the primary aim of this study was to determine if these proteins contribute to pathogenicity. Our secondary aim was determine if they are secreted coat proteins. Here we report that all neonatal mice infected with a wild-type strain of C. rodentium perished. In contrast a cexE mutant was significantly attenuated with 45% neonate survival. In adult mice the wild-type strain reached significantly higher loads in the large intestines and were shed in greater numbers than cexE mutants. Secretion of the CexE homolog in EAEC is dependent upon an atypical Type I secretion system that accepts its client from the periplasm rather than the cytoplasm. Insertion mutants of cexC, the putative ATPase of the CexE secretion system, were attenuated in our murine model. In vitro we found that CexC is required for the secretion of CexE to the outer membranes of both ETEC and C. rodentium. Secretion is not constitutive because CexE accumulates in the periplasm when the two pathogens are cultured under noninducing conditions. Although secretion conditions differ between ETEC and C. rodentium, secreted CexE remains predominantly associated with the outer membranes of both species. In aggregate these findings demonstrate that CexE is a secreted coat protein and virulence factor that promotes colonization of host intestinal tissues by enteric pathogens.

CexE是一种12 kDa的蛋白质，最初据报道仅在三种产肠毒素的菌株中存在 大肠杆菌（ETEC）；世界范围内引起腹泻疾病的常见原因。但是，对测序基因组的检查表明，大多数ETEC菌株中实际上都存在CexE。此外，CexE的同源物存在于肠聚合反应中大肠杆菌 （EAEC）， 小肠结肠炎耶尔森菌， 普罗维登西亚和 啮齿类柠檬酸杆菌。尽管已经假设CexE及其同源物是毒力因子，但这尚未得到检验。因此，这项研究的主要目的是确定这些蛋白质是否有助于致病性。我们的次要目的是确定它们是否分泌外壳蛋白。在这里，我们报告所有感染了野生型啮齿动物死了 相比之下CEXE突变体显着减弱，新生儿存活率为45％。在成年小鼠中，野生型毒株在大肠中的负荷明显更高，并且脱落的数量比CEXE突变体。EAEC中CexE同源物的分泌取决于非典型的I型分泌系统，该系统从周质而非细胞质接受其客户。的插入突变体CEXC，在我们的鼠模型中减弱了CexE分泌系统的假定ATPase。 体外 我们发现CexC是分泌Eex和ETEC外膜的CexE所必需的 啮齿动物。分泌不是组成性的，因为当在非诱导条件下培养两种病原体时，CexE会在周质中积累。尽管ETEC和啮齿动物，分泌的CexE仍然主要与两个物种的外膜相关。总体而言，这些发现表明CexE是一种分泌的外壳蛋白和致病因子，可促进肠道病原体对宿主肠道组织的定植。