2013 Fiscal Year Final Research Report
Salmonella effector GogA induces caspase-8 activation, leading to modulation of proinfallamatory response in macrophages
| Project/Area Number |
23689026
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| Research Category |
Grant-in-Aid for Young Scientists (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Bacteriology (including Mycology)
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| Research Institution | Chiba University |
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Principal Investigator |
TAKAYA Akiko 千葉大学, 薬学研究科(研究院), 准教授 (80334217)
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| Co-Investigator(Renkei-kenkyūsha) |
YAMAMOTO Tomoko 千葉大学, 大学院薬学研究院, 教授 (60110342)
SATO Yoshiharu 千葉大学, 大学院薬学研究院, 助教 (00554586)
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| Project Period (FY) |
2011-11-18 – 2014-03-31
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| Keywords | サルモネラ / カスパーゼ－8 / 炎症反応 / 細胞死 / エフェクター |
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| Research Abstract |
Caspase-8 activation requires tight regulation owing to its two opposing functions, namely as an initiator of apoptosis and in a non-apoptotic role including induction of the pro-inflammatory response. We have demonstrated that a novel Salmonella effector GogA induces caspase-8 activation. The limited caspase-8 activation by GogA is involved in NFkB activation, leading to modulation of proinflammatory cytokines at the early stage of Salmonella infection. However, caspase-8 activation is not involved in induction of pyroptosis. Furthermore, caspase-8 activation by GogA may be required for interaction with LSm8, U6 snRNA-associated Sm-like protein. On the other hand, Salmonella has another effector involving in caspase-8 activation in addition of GogA. These finding together, it is suggested that induction of NFkB activation by the activated-caspase-8 are regulated through translocation of some effectors including GogA, leading to proliferation of Salmonella within host cells.
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