| Project/Area Number |
25871000
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Bacteriology (including mycology)
Laboratory animal science
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| Research Institution | Fukuoka University |
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Principal Investigator |
ITOH Ryota 福岡大学, 医学部, 助教 (70403920)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | クラミジア / カルパイン / 阻害剤 / 感染症 / 免疫 |
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| Outline of Final Research Achievements |
The obligate intracellular pathogens Chlamydiae replicates within a membrane-bound vacuole termed inclusion and acquire the nutrients from infected cells. For optimal chlamydial growth, prompt modifications of host intracellular environment is indispensable. Here we show that some inhibitors for the calcium-activated protease calpain dramatically affect in both chlamydial growth and host immunological responses. Calpain inhibitor MDL28170 suppress nuclear localization of the transcription factor NF-kB p65 (RelA) and strictly down-regulates both mRNA expressions and proteins secretions of inflammatory cytokines such as IL-1α, IL-1β and IL-6 from Chlamydia-infected murine macrophages. Several calpain inhibitors MDL28170, calpeptin, ALLN and MG132 exclusively regulates chlamydial growth and contains similar dipeptide structures. Our results suggested the possibility of some calpain inhibitors such as MDL28170 or calpeptin for therapeutic usage to the chlamydial infectious disease.
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