Gort A S, Miller V L
Department of Molecular Microbiology and Division of Infectious Disease, Washington University School of Medicine, and St. Louis Children's Hospital, St. Louis, Missouri 63130, USA.
Infect Immun. 2000 Dec;68(12):6633-42. doi: 10.1128/IAI.68.12.6633-6642.2000.
Yersinia enterocolitica is one of three pathogenic Yersinia species that share a tropism for lymphoid tissues. However, infection of an immunocompromised host is likely to result in a systemic infection, which is often fatal. Little is known about the bacterial proteins needed to establish such an infection. The genes that encode these virulence factors are likely to be active only during systemic infection. A library of random cat fusions was used to inoculate BALB/c mice. Fusions expressed during a systemic infection were enriched by the administration of chloramphenicol-succinate. Y. enterocolitica isolates recovered from the mice were tested for chloramphenicol resistance in vitro. Fusions that were inactive in vitro were analyzed further and found to represent 31 allelic groups. Each was given a sif (for systemic infection factor) designation. Based on homology to known proteins, the sif genes are likely to encode proteins important for general physiology, transcription regulation, and other functions. During systemic infections, 13 of the sif-cat fusions were able to outcompete the wild type in the presence of chloramphenicol-succinate, confirming that the fusions were active. The in vitro expression of several sif genes was determined, showing modest changes in response to various growth conditions. A mutation in sif15, which encodes a putative outer membrane protein, caused attenuation during systemic infection but not during colonization of the Peyer's patches. Comparisons between the Y. enterocolitica sif genes and the previously identified hre genes imply that very different groups of genes are active during a systemic infection and during colonization of the Peyer's patches.
小肠结肠炎耶尔森菌是三种对淋巴组织具有嗜性的致病性耶尔森菌之一。然而，免疫功能低下宿主的感染很可能导致全身感染，这种感染往往是致命的。对于建立这种感染所需的细菌蛋白了解甚少。编码这些毒力因子的基因可能仅在全身感染期间活跃。利用随机cat融合文库接种BALB/c小鼠。通过给予琥珀酸氯霉素富集在全身感染期间表达的融合体。对从小鼠体内回收的小肠结肠炎耶尔森菌分离株进行体外氯霉素抗性测试。对在体外无活性的融合体进行进一步分析，发现它们代表31个等位基因群。每个等位基因群都被赋予了一个sif（全身感染因子）名称。基于与已知蛋白质的同源性，sif基因可能编码对一般生理学、转录调控和其他功能重要的蛋白质。在全身感染期间，13个sif-cat融合体在存在琥珀酸氯霉素的情况下能够胜过野生型，证实这些融合体是活跃的。测定了几个sif基因的体外表达，结果显示其表达随各种生长条件有适度变化。sif15编码一种假定的外膜蛋白，该基因的突变在全身感染期间导致毒力减弱，但在派伊尔结定植期间没有这种情况。小肠结肠炎耶尔森菌sif基因与先前鉴定的hre基因之间的比较表明，在全身感染和派伊尔结定植期间，活跃的基因群有很大差异。
