Section of Microbial Pathogenesis, Yale University School of Medicine, Boyer Center for Molecular Medicine, 295 Congress Ave., New Haven, CT 06536, USA.
Infect Immun. 2010 Aug;78(8):3540-53. doi: 10.1128/IAI.00109-10. Epub 2010 Jun 1.
Campylobacter jejuni is the leading cause of infectious gastroenteritis in industrialized nations. Its ability to enter and survive within nonphagocytic cells is thought to be very important for pathogenesis. However, little is known about the C. jejuni determinants that mediate these processes. Through an extensive transposon mutagenesis screen, we have identified several loci that are required for C. jejuni efficient entry and survival within epithelial cells. Among these loci, insertional mutations in aspA, aspB, and sodB resulted in drastic reduction in C. jejuni entry and/or survival within host cells and a severe defect in colonization in an animal model. The implications of these findings for the understanding of C. jejuni-host cell interactions are discussed.
空肠弯曲菌是工业化国家感染性胃肠炎的主要病原体。它能够进入和在非吞噬细胞中存活被认为对其发病机制非常重要。然而，关于介导这些过程的空肠弯曲菌决定因素知之甚少。通过广泛的转座子诱变筛选，我们已经鉴定出几个空肠弯曲菌有效进入和在肠上皮细胞中存活所必需的基因座。在这些基因座中，aspA、aspB 和 sodB 的插入突变导致空肠弯曲菌进入和/或宿主细胞内存活的急剧减少，并且在动物模型中的定植严重缺陷。这些发现对理解空肠弯曲菌与宿主细胞的相互作用具有重要意义。
