| Project/Area Number |
12670268
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Bacteriology (including Mycology)
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| Research Institution | Aichi Medical University |
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Principal Investigator |
YOSHIDA Tomoaki Aichi Med. Univ., Dept of Microbiology and Immunology, Associate professor, 医学部, 助教授 (70210705)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 2001: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2000: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | Enterohemorrhagic E. coli / Colon epithelial cells / Intracelluar invasion / Type 3 secretion / Cytoskeleton / 細胞内感染 / インティミン / type III分泌 / typeIII分泌 |
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| Research Abstract |
The purpose of this project is to elucidate the infection mechanism of enterohemorrhagic E. coli O157 to human intestinal epithelial cells.
1) The primary culture of native epithelial cells from human colon has been established.
2) E. coli O157 has been shown to invade the native colon epithelial cells to a comparable extent with Salmonella enterica as proved by killing the extracellular bacteria by gentamicin. The invasion was dependent on the action of cytoskeletons and cell surface cholesterol content.
3) The morphological insights using con focal fluorescent microscopy and electromicroscopy confirmed the intracellular bacteria, in addition to gentamicin protection assay.
4) The target cells of E. coli O157 were shown to express epithelial markers but not monocyte markers.
5) When another type of epithelial cell, Hela was tested for the infection of E. coli 0157 and salmonella, the latter invaded to a similar degree of colon cells but not the former.
6) Employing the isogenic deletion mutants of bacterial effacement locus, the sepL was proved to be essential for the invasion activity, whereas not was eaeA, espA or Tir.
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