Activation of inflammasome by Streptococcus sanguinis

2015 Fiscal Year Final Research Report

• Project/Area Number: 26861566
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Pathobiological dentistry/Dental radiology
• Research Institution: Hokkaido University
• Principal Investigator: SAEKI Ayumi 北海道大学, 歯学研究科(研究院), 助教 (70638345)
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: 口腔連鎖球菌 / インフラマゾーム

Outline of Final Research Achievements

S. sanguinis induced release of IL-1βby a murine dendritic cell (XS-106) and a murine bone marrow-derived macrophage (BMM) from C57BL/6, but not by BMMs from caspase-1-, ASC- and NLRP3-deficient mice. Cytochalasin D, an inhibitor of actin polymerization, inhibited phagocytosis of S. sanguinis and reduced the IL-1β-inducing activity in XS106. The receptor P2X (P2XR)/P2YR inhibitor oxidized ATP, the P2X7R selective inhibitor KN-62 and the ATP-degradting enzyme apyrase downregulated IL-1βrelease in XS106.
Thus, this study suggests that S. sanguinis activates NLRP3 inflammasome to induce IL-1βrelease by murine dendritic cells and macrophages, and phagocytosis of the organism, interaction of ATP and its derivatives with P2X7 and P2Y receptors are involved in the expression of the activity.

Free Research Field

歯学