2020 Fiscal Year Final Research Report
njury protection through a novel inflammasome signaling pathway against acute lung injury
| Project/Area Number |
19K18274
|
|---|
| Research Category |
Grant-in-Aid for Early-Career Scientists
|
| Allocation Type | Multi-year Fund |
|---|
| Review Section |
Basic Section 55050:Anesthesiology-related
|
|---|
| Research Institution | Tottori University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2019-04-01 – 2021-03-31
|
| Keywords | 急性肺傷害 / 上皮バリア機能 |
|---|
| Outline of Final Research Achievements |
The epithelial tight junctions (TJs) are essential for the epithelial barrier function that seals the intercellular and intracellular space.
In this study, we investigated whether activation of the inflammasome before acute inflammatory injury could suppress the disruption of epithelial barrier function caused by acute injury. As a result, lung injury and liver injury induced by high-concentration of LPS and disappear of TJs were suppressed by pretreatment with low-concentration LPS. In cultured epithelial cells, low-dose LPS mediated inflammasome activation suppressed the disappearance of TJs by calcium depletion. However, this effect was canceled by inhibited of inflammasome activation.
The present results indicated that the inflammasome signal is involved in the protection of epithelial barrier function.
|
| Free Research Field |
細胞生物学
|
| Academic Significance and Societal Importance of the Research Achievements |
インフラマソームの活性化に関する既存の報告の多くは炎症応答による細胞傷害についての解析であった。本研究は、細胞傷害保護に作用する新規インフラマソームシグナル経路の存在に着目し検討した。弱い炎症刺激によるインフラマソームの活性化が上皮バリア機能の保護に働くことが明らかとなった。敗血症、急性肺傷害、感染、癌の進展などに共通した分子病態として上皮バリア機能の破綻が生じる。インフラマソームの活性化は、上皮バリア機能の破綻を抑制できることから、それら病態の治療や予防の確立に本研究が貢献できる可能性が期待できる。
|
