2001 Fiscal Year Final Research Report Summary
Susceptibility to bacterial infection by gene transfection of beta defensinsjnto oral epithelial cells
| Project/Area Number |
12671777
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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 |
Morphological basic dentistry
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| Research Institution | Health Scjences University of Hokkaido |
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Principal Investigator |
ABIKO Yoshihiro Health Scjences University of Hokkaido, Dentistry, Associate Professor, 歯学部, 助教授 (90260819)
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| Co-Investigator(Kenkyū-buntansha) |
ARAKAWA Toshiya Health Scjences University of Hokkaido, Dentistry, Associate Professo, 歯学部, 講師 (40306254)
NAKAJIMA Keisuke Health Scjences University of Hokkaido, Dentistry, Associate Professor, 歯学部, 助教授 (80227785)
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| Project Period (FY) |
2000 – 2001
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| Keywords | defensin / transfection / bacterial infection / periodontitis |
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| Research Abstract |
βDefensins (hBD) are a group of antimicrobial peptides. We have demonstrated the decreasing expression of hBDs in KB cells widely used in vitro model of periodontitis, and that Actinobacillus actinomycetemcomitant (Aa) infected into the KB cells to induce their apoptosis. The study examined whether overexpression of hBDs in KB cells by the gene transfection made them resistance to bacterial infection. We established hBD-1-and hBD-2- overexpressed KB cell lines (KB-hBD1, KB-hBD2) by gene transfection. The mRNA and protein expressions of hBDs were confirmed by RTPCR and western blot analyses, respectively. The western blot analysis showed double bands, implying that processing occurred during production of the functional protein. DNA fragmentation assay was carried out to evaluate the infected rate. The DNA fragmentation in control KB cells increased with Aa infection in a dose dependent manner. On the other hand, no significant increase of DNA fragmentation in KB-hBD1 or KB-hBD2 with Aa infection was observed. The infection rate in KB-hBD1 or KB-hBD2 was a significantly lower than control KB. The infection rate in KB-hBD1 is a significantly higher than that in KB-hBD2. These results suggest that overexpression of hBDs in epithelial cells makes them resistance to bacterial infection.
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