2014 Fiscal Year Final Research Report
Role of the inflammasome in bacterial infections
Project/Area Number |
23590504
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Bacteriology (including Mycology)
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Research Institution | Kyoto University |
Principal Investigator |
TSUCHIYA Kohsuke 京都大学, 医学(系)研究科(研究院), 助教 (50437216)
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Project Period (FY) |
2011-04-28 – 2015-03-31
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Keywords | インフラマソーム / ASC / NLRP3 / 細菌感染 / リステリア / 肺炎球菌 |
Outline of Final Research Achievements |
Inflammasomes are innate immune mechanisms that activate caspase-1 in response to various stimuli, including microbial pathogens. Once activated, inflammasomes induce the production of pro-inflammatory cytokines and programmed cell death through caspase-1. Accumulating data have suggested inflammasomes play a protective role against microbial infections. In this study, we examined the mechanism and role of inflammasome formation in infection with two Gram-positive bacteria. We found that Streptococcus pneumoniae is recognized by the cytosolic DNA receptor AIM2, which in turn forms an inflammasome complex to activate caspase-1. It was also found that inflammasomes are critical for host defense against pneumococcal pneumonia. On the other hand, inflammasomes were detrimental to the host in lethal infection with Listeria monocytogenes. Our study revealed that inflammasomes can be upstream of an immunosuppressive response, which may explain the detrimental effect of inflammasomes.
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Free Research Field |
細菌学・免疫学・感染免疫
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