| Project/Area Number |
10470252
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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 |
Digestive surgery
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| Research Institution | Tohoku University |
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Principal Investigator |
FUKUSHIMA Kouhei Tohoku University, Graduate School of Medicine, Research Associate, 大学院・医学系研究科, 助手 (20271900)
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| Co-Investigator(Kenkyū-buntansha) |
SASAKI Iwao Tohoku Univ, Graduate School of Med, Professor, 大学院・医学系研究科, 教授 (60125557)
NAITO Hiroo Tohoku Univ, Hospital, Lecture, 医学部附属病院, 講師 (90180223)
FUNAYAMA Yuji Tohoku Univ, Hospital, Lecture, 医学部附属病院, 講師 (50192315)
OHTANI Haruo Tohoku Univ, Graduate School of Med, Associate Professor, 大学院・医学系研究科, 助教授 (30133987)
笹野 公伸 東北大学, 大学院・医学系研究科, 教授 (50187142)
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥12,900,000 (Direct Cost: ¥12,900,000)
Fiscal Year 2000: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1999: ¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 1998: ¥8,600,000 (Direct Cost: ¥8,600,000)
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| Keywords | epithelial cell / inflammatory bowel disease / Ulcerative colitis / germ-free / クーロン病 / 炎症性腸疾患 |
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| Research Abstract |
A total of 300 displays with different sets of primers were carried out. Bands were selected after at least 2 displays using the same combination of primers. Some genes such as reg IIIβ, IIIγ and carbonic anhydrase I were selected in multiple displays with different sets of primers. We successfully cloned 118 bands. Sixty-eight clones out of 118 (58%) were used as probes in northern blotting to confirm differential gene expression among GF, bacteria-reconstituted and specific pathogen-free (SPF) mice, or between the small intestine and the colon. To evaluate the significance and specificity of gene modulation in the bacterial reconstitution model, we established dextran sulfate sodium (DSS) induced-colitis as an inflammatory control. RNAs from DSS-colitis were also used in some experiments.
We clearly demonstrate in the following that our bacterial reconstitution model and epithelial gene screening truly detects human genes associated with IBD, suggesting that some genes listed in table 1 and 2 must be involved in human IBD.
We concentrated two molecules. We demonstrated epithelial induction of serum amyloid A(SAA) in IBD and modulatory activity of SAA in LPS-associated inflammation. We additionally showed epithelial induction of Regenerating gene III and HIP/PAP in experimental and human inflammatory bowel disease in association with Paneth cell metaplasia.
In summary, we successfully identified genes modulated in human IBD by analyzing bacteria reconstitution model and investigating human homologues
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