| Project/Area Number |
17390559
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Periodontal dentistry
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| Research Institution | Osaka University |
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Principal Investigator |
AMANO Atsuo Osaka University, Graduate School ofDentisty, Department of Oral Frontier Biology, Professor (50193024)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAGAWA Ichiro The University of Tokyo, The Institute of Medical Science, Division of Bacteriology, Department of Infectious Disease Control, International Research Center for Infectious Diseases, Associate Professor (70294113)
INABA Hiroaki Osaka University, Graduate School ofDentisiry, Dept of Oral Frontier Biology, Assistant Professor (70359850)
KAWAI Shinji Osaka University, Graduate School ofDentisiry, Dept of Oral Frontier Biology, Assistant Professor (40362678)
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| Project Period (FY) |
2005 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥16,210,000 (Direct Cost: ¥15,400,000、Indirect Cost: ¥810,000)
Fiscal Year 2007: ¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2006: ¥5,500,000 (Direct Cost: ¥5,500,000)
Fiscal Year 2005: ¥7,200,000 (Direct Cost: ¥7,200,000)
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| Keywords | Dentistry / Bacteria / Infection / Cell・tissue / Signal transduction / Porphyromonas gingivalis / 細胞内侵入細菌 / 歯周病 / リピッドラフト / エンドサイトーシス / マイクロアレイ / dynamin |
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| Research Abstract |
Porphyromonas gingivalis is a predominant periodontal pathogen that expresses a number of potential virulence factors involved in the pathogenesis of periodontitis. Gingival epithelial cells are spontaneously exposed to bacterial attacks and function to prevent invasion by bacteria into deeper tissues. P. gingivalis fimbriae are a critical factor for mediation of interaction of the organism with host tissues, as they promote both bacterial adhesion to and invasion of targeted sites. Fimbriae are capable of binding to human salivary components, extracellular matrix proteins, and commensal bacteria, while they also strongly adhere to cellular a581-integrin. Following adhesion to a581-integrin, P. gingivalis is captured by cellular pseudopodia, which enables invagination through an actin-mediated pathway. The invasive event has been reported to require host cellular dynamin, actin fibers, microtubules, and lipid rafts. Following passage through the epithelial barrier, the intracellular pathogen impairs cellular function. Fimbriae are classified into 6 genotypes (types I to V and Ib) based on the diversity of the fimA genes encoding each fimbria subunit, and intracellular P. gingivalis with type II fimbriae has been found to clearly degrade integrin-related signaling molecules, paxillin, and focal adhesion kinase, which disables cellular migration and proliferation. These events are considered to integrate the bacterial strategy for persistence in periodontal tissues.
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