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Effects of a novel pathogenicity-related gene product of Salmonella, SEp22, on the viability of Salmonella in its environments

沙门氏菌新型致病性相关基因产物 SEp22 对沙门氏菌在环境中生存力的影响

基本信息

批准号：
15590117
负责人：
AMANO Fumio
金额：
$ 2.3万
依托单位：
Osaka University of Pharmaceutical Sciences
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2003
资助国家：
日本
起止时间：
2003 至 2004
项目状态：
已结题

项目摘要

Mechanisms underlying regulation of SEp22 expression were further studied in pathogenic strains of Salmonella Enteritidis, isolated from poultry farms. Expression of SEp22 was dependent on the growth phases in nutritionally enriched culture medium like Luria-Bertani medium(LB), and was scarce in logarithmic phase but became rapidly increased in late-logarithmic to stationary phases. Northern blot or RT-PCR analysis of SEp22 mRNA revealed that it increased prior to the synthesis of SEp22 protein but slightly later than the increase of RNA polymerase σ factor, σ32, expression in these growth phases. However, expression of σ70 was not related with SEp22. These changes in SEp22 were cyclically repeated by transferring Salmonella into fresh LB. In contrast, induction of SEp22 was not observed even in stationary phases when cultured in nutritionally poor medium like M-9 medium, which was in part restored by addition of LB to M-9 medium. We have been examining the nutrition factor(s) in LB which supports induction of SEp22 under these conditions, and have excluded glucose or some amino acids from such factor(s). Taken together, these results suggest that expression of SEp22 is transcriptionally regulated and that environmental isolate of Salmonella, even if it potentially causes pathogenicity to host animals, does not always become pathogenic in nutritionally poor environment due to lack of expression of SEp22.

进一步研究了从家禽养殖场分离的肠炎沙门氏菌的致病株对SEp22表达的调控机制。在Luria-Bertani(Luria-Bertani，Luria-Bertani)等营养丰富的培养基中，SEp22的表达随生长阶段的不同而变化，在对数生长期很少，但在对数后期到稳定期迅速增加。Northern印迹和RT-PCR法分析表明，在这些生长阶段中，SEP22蛋白合成之前表达增加，但略晚于RNA聚合酶σ因子σ32表达的增加。而σ70的表达与SEP2 2无关。通过将沙门氏菌转移到新鲜的LB中，SEp22中的这些变化被循环重复。相反，在营养较差的M-9培养基中，即使在静止相也没有观察到SEp22的诱导，而在M-9培养基中添加LB可以部分恢复这种诱导。我们一直在检测在这些条件下支持SEP22诱导的LB中的营养因子(S)，并排除了葡萄糖或一些氨基酸(S)。综上所述，这些结果表明SEp22的表达是转录调控的，环境分离的沙门氏菌即使可能导致宿主动物致病，也不总是因为缺乏SEp22的表达而在营养不良的环境中致病。