| Project/Area Number |
10670269
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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 | Kitasato University |
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Principal Investigator |
OKADA Nobuhiko Kitasato Univerisity School of Parmaceutical Science, Associate Professor, 薬学部, 助教授 (80194364)
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| Co-Investigator(Kenkyū-buntansha) |
KIKUCHI Yuji The Kitasato Institute, Laboratory of Molecullar Immunology, Chief Researcher, 室長 (60262078)
DANBARA Hirofumi Kitasato Univerisity School of Parmaceutical Science, Professor, 薬学部, 教授 (40114558)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 1999: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1998: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | Salmonella infection / Citekines / Bacterial invasion / Endothelial cells / Vieulence factors / Adhesion molecules |
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| Research Abstract |
Salmonella infection of human vascular endothelial cells and its role of as a stimulus for endothelial cell activation have been studies. Invasion of cultured HUVEC monolayers was dependent of the Salmonella invasion locus, Salmonella pathogenicity island 1 (SPI-1). The wild-type RF-1 strain of Salmonella enterica serovar Choleraesuis was efficiently internalized by HUVEC whereas the invasiveness of an isogenic invA mutant decreased to 30% of the wild-type strain. When analyzed by a reverse transcriptase PCR method, infection of HUVEC with invasive, but not noninvasive, bacteria resulted in increased expression of mRNA for the cytokine IL-8. In addition, Salmonella stimulated surface expression of E-selectin (CD62E), ICAM-1 (CD54) and VCAM-1 (CD106). These results may indicate that invasion of endothelial cells by Salmonella is a mechnisms for triggering local vascular inflammation.
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