| Project/Area Number |
14370582
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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 |
Morphological basic dentistry
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| Research Institution | Osaka University |
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Principal Investigator |
KAWABATA Shigetada Dentistry, Microbiology, Associate Prof., 大学院・歯学研究科, 助教授 (50273694)
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| Co-Investigator(Kenkyū-buntansha) |
OKAMOTO Shigefumi Dentistry, Microbiology, Assistant Prof., 大学院・歯学研究科, 助手 (50311759)
NAKAGAWA Ichiro Dentistry, Microbiology, Assistant Prof., 大学院・歯学研究科, 講師 (70294113)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥11,500,000 (Direct Cost: ¥11,500,000)
Fiscal Year 2003: ¥4,000,000 (Direct Cost: ¥4,000,000)
Fiscal Year 2002: ¥7,500,000 (Direct Cost: ¥7,500,000)
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| Keywords | S.pyogenes / invasion / surface protein / fibronectin / pinding / Streptococcus pyogenes / 細胞侵入 / 細胞付着 / 遺伝子 / ワクチン / ゲノム / 劇症型レンサ球菌感染症 / Streptococuus pyogenes / 付着 |
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| Research Abstract |
Group A Streptococcus pyogenes (GAS) has surface-located fibronectin (Fn)-binding proteins known to be a major virulence factor, which adhere to and invade host cells. We present a novel Fn-binding protein of GAS serotype M3 and M18 strains isolated from patients with toxic shock-like syndrome (TSLS). By searching the whole genome sequence of an M3 strain from a TSLS patient, an open reading frame was found among the putative surface proteins. It possessed an LPXTG motif and Fn-binding repeat domains in the C-terminal region, and was designated as FbaB (Fn-binding protein of group A streptococci type B). The fbaB gene was found in all M3 and M18 strains examined, though not in other M serotypes. Furthermore, FbaB protein was expressed on the cell surface of TSLS strains but not on non-TSLS ones. ELISA and ligand blotting revealed that recombinant FbaB exhibits a strong Fn-binding ability. An FbaB-deficient mutant strain showed 6-fold lower adhesion and invasion efficiencies to HEp-2 cells than the wild type. Moreover, mortality was decreased in mice infected with the mutant strain in comparison to the wild type. These data suggest that FbaB is etiologically involved in the development of invasive streptococcal diseases.
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