| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| 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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