| Budget Amount *help |
¥3,920,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥420,000)
Fiscal Year 2007: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2006: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Research Abstract |
In a pathogenic strain of Salmonella Enteritidis, (SE), sep22 gene was transcribed very little in early logarithmic phase, then became gradually increased in accordance with the bacterial growth, reaching maximal at the late logarithmic phase usually 6-8 h after inoculation of the bacteria in to fresh LB medium. On the other hand, a typical virulent factor of Salmonella, invA, which is also an important member of Type III secretion system (TTSS), became rapidly expressed after starting cultivation of the bacteria, and became maximal usually 1-2 h after incubation, followed by gradual decrease until stational phase. These results suggest that sep22 and invA show quite distinct regulation in a pathogenic Salmonella cell, which should exert different roles during establishing infection of Salmonella to host cells, i.e., the former, working as a protective factor against killing effector molecules from the host., and the latter, working as an offense factor toward the host. Some trials to prove the pivotal role of sep22 in Salmonella infection are in progress to establish revertants using KO-5 strain, a sep22-gene knock out mutant of SE. Regarding nutritional factors involved in SEp22 expression, we characterized some of them in LB medium, casamino acids, cabbage extracts, fetal bovine serum, egg yolk and so on. A variety of molecules were shown to be effective as a nutritional factors, and some molecules in casamino acids have been purified using HPLC. Besides, SEp22 protein expression in SE strains was shown to be playing negative roles in adhesion of pathogenic SE to macrophages but also positive roles in invasion to the macrophages, although that in SE showed no significant differences in the course of SE infection to Caco-2 cells, suggesting multiple regulatory roles of SEp22 in Salmonella pathogenesis.
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