| Project/Area Number |
12670505
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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 |
Gastroenterology
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| Research Institution | Yokohama City University |
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Principal Investigator |
TANAKA Katsuaki Yokohama City University Hospital Professor, 医学部附属病院, 教授 (10201617)
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| Project Period (FY) |
2000 – 2002
|
| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2002: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2001: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | Hepatics C virus / Interferon receptor / IFNARI / IFNAR2 |
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| Research Abstract |
Intrahepatic mRNA levels of type-I interferon receptor genes have been shown to correlate with the clinical efficacy of interferon therapy in patients with chronic hepatitis C. Therefore, we first attempted to raise efficiency of interferon for excluding the hepatitis C virus by expressing the interferon receptor genes into the human hepatocyte cell lines. Then, the factor with the possibility of up-regulating the interferon receptor was retrieved. We found that lactoferrin supplementation significantly improved the biochemical and virological responses at the end of interferon treatment in patients with chronic hepatitis C; however, it did not change the PBMC's and the hepatic mRNA levels of type-I interferon receptor genes. Far-Western blot analysis using the lactoferrin fragments and the hepatitis C virus E2 protein revealed the 33 amino acid residues as the minimum binding site in the carboxy1 region of lactoferrin. We furthermore investigated the mechanism of anti-inflammation action of lactoferrin using rat model of acute hepatic failure, and found that plasma and hepatic TNF-α mRNA levels were decreased in rats pretreated by lactoferrin. Lactoferrin is a promising candidate for adjuvant therapy with interferon in patients with chronic hepatitis C through its anti-virus and the anti-inflammatory action.
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