| Project/Area Number |
24791022
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Infectious disease medicine
|
|---|
| Research Institution | Osaka University |
|---|
Principal Investigator |
NAKAYAMA Tatsuya 大阪大学, グローバルコラボレーションセンター, 特任助教 (80552158)
|
|---|
| Project Period (FY) |
2012-04-01 – 2015-03-31
|
| Project Status |
Completed (Fiscal Year 2014)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
|---|
| Keywords | 豚連鎖球菌 / コレステロール依存性細胞溶解毒素 / スイリシン / 腸管感染 |
|---|
| Outline of Final Research Achievements |
The aim of this study is to investigate how S. suis disrupts intestinal cells and translocates from the gut to the blood circulation. In mouse model, the wild-type (WT) S. suis strain or the suilysin gene-knockout (Δsly) S. suis strain with FITC-dextran (FD) was inoculated to the intestinal loop. The number of bacteria in the blood and the translocation of FD from the intestinal lumen to the blood stream were determined in mice after WT strain inoculation. Moreover, the WT strain prompted a higher expression of pro-inflammatory cytokines than theΔsly strain did. The mechanisms of disrupt intestinal cell was investigated by using transwell system. The cell barrier was rapidly disrupted by infection with WT strain. Besides, it found that low SLY concentration performed to make a hole in the cell, and influenced the cytoskeleton, while SLY induced calpain which attenuated paracellular proteins. Based on these findings, SLY helps S. suis to disrupt intestinal cell barrier.
|
