| Project/Area Number |
15390223
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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 |
Gastroenterology
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| Research Institution | Asahikawa Medical College |
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Principal Investigator |
KOHGO Yutaka Asahikawa Medical College, Medicine, Professor (10133183)
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| Co-Investigator(Kenkyū-buntansha) |
ASHIDA Toshifumi Asahikawa Medical college, Medicine, Assistant Professor (50261409)
AYABE Tokiyosi Asahikawa Medical college, Medicine, Assistant Professor (90301019)
OTAKE Takaaki Asahikawa Medical college, Medicine, Instractor (10359490)
FUJIYA Mikihiro Asahikawa Medical college, Medicine, Instractor (80322915)
前本 篤男 旭川医科大学, 医学部, 寄附講座教員 (40400113)
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| Project Period (FY) |
2003 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥14,300,000 (Direct Cost: ¥14,300,000)
Fiscal Year 2006: ¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 2005: ¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 2004: ¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 2003: ¥6,900,000 (Direct Cost: ¥6,900,000)
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| Keywords | Inflammatory Bowel Disease / Antibacterial peptides / Innate immunity / Crohn's disease / Alpha-defensins / Himan defensin 5 / 内因性抗菌ペプチド / 潰瘍性大腸炎 / デフェンシン / 粘膜免疫 / ディフェンシン / 病原体認識 |
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| Research Abstract |
The aim of this study was to determine the role of antibacterial peptides in normal and inflamed intestine, and explore a potential therapeutic option for inflammatory bowel disease through the regulation of innate immunity by recombinant defensins.
As results, this study demonstrated that, 1) human defensin 5 (HD-5) mRNA and protein expressed in small intestinal crypts of healthy volunteers and patients with Crohn's disease (CD) and ulcerative colitis, 2) gene profiles of defensins and toll-like receptors in the patients with CD was different from that in healthy volunteers, 3) bactericidal activity of HD-5 derived from the patients with CD was attenuated compared with that of healthy volunteers, 4) whereas the amino acid sequence of proHD-5 extracted from the patients with CD, disulphide bridges of the HD-5 of some CD patients were disappeared, suggesting that the function of HD-5 was regulated by a post-translational modification in inflammatory bowel disease and 5) recombinant HD-5, which was stable for trypsins and proteases, improved the survival rate of mice treated with 4% dextran sodium sulfate-treated.
In summary, this study provided an important role of HD-5 in innate immunity of normal and inflamed inteastine, and proposed a novel therapeutic option for inflammatory bowel disease, targeting the impaired innate immunity.
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