Elucidation of intestinal mucosal immune system through the intracellular processing mechanisms of bacteria and its application for novel therapy of inflammatory bowel disease
| Project/Area Number |
20200080
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| Research Category |
Grant-in-Aid for Scientific Research on Innovative Areas (Research a proposed research project)
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| Allocation Type | Single-year Grants |
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| Research Field |
Gastroenterology
Immunology
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| Research Institution | Keio University |
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Principal Investigator |
INOUE Nagamu Keio University, 医学部, 講師 (00232546)
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| Co-Investigator(Kenkyū-buntansha) |
OKAMOTO Susumu 慶應義塾大学, 医学部, 講師 (70255446)
HISAMATSU Tadakazu 慶應義塾大学, 医学部, 講師 (60255437)
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| Co-Investigator(Renkei-kenkyūsha) |
HIBI Toshifumi 慶應義塾大学, 医学部, 教授 (50129623)
WATANABE Mamoru 東京医科歯科大学, 大学院・医歯学総合研究科器官システム制御学系消化器病態学, 教授 (10175127)
MORIMOTO Chikao 東京大学, 医科学研究所先端医療研究センター免疫病態分野, 教授 (30119028)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥33,800,000 (Direct Cost: ¥26,000,000、Indirect Cost: ¥7,800,000)
Fiscal Year 2010: ¥11,050,000 (Direct Cost: ¥8,500,000、Indirect Cost: ¥2,550,000)
Fiscal Year 2009: ¥11,050,000 (Direct Cost: ¥8,500,000、Indirect Cost: ¥2,550,000)
Fiscal Year 2008: ¥11,700,000 (Direct Cost: ¥9,000,000、Indirect Cost: ¥2,700,000)
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| Keywords | 炎症性腸疾患 / 粘膜免疫 / 腸内細菌 / マクロファージ / クローン病 / オートファジー / 自然免疫 / 細胞内寄生菌 |
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| Research Abstract |
We tried to elucidate the roles of macrophages in intestinal inflammation by using an IL-10-deficient (IL-10-/-) mouse colitis model, and demonstrated that abnormally differentiated subsets of intestinal macrophage play a key role in Th1-dominant chronic colitis through excess production of IL-12 and IL-23 in response to bacteria. Moreover, we found that lamina propria macrophages (LPMs) could be separated into two subsets with distinct side-scattered properties. LPM2 subset migrated in response to MCP-1 and produced a larger amount of IL-10 in response to commensal bacteria.
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Report
(4 results)
Research Products
(22 results)
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[Journal Article] Competition between colitogenic Th1 and Th17 cells contributes to the amelioration of colitis.2010
Author(s)
Mikami Y, Kanai T, Sujino T, Ono Y, Hayashi A, Okazawa A, Kamada N, Matsuoka K, Hisamatsu T, Okamoto S, Takaishi H, Inoue N, Ogata H, Hibi T
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Journal Title
Eur J Immunol 40(9)
Pages: 2409-2422
Related Report
Peer Reviewed
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[Journal Article] Exacerbating role of gammadelta T cells in chronic colitis of T-cell receptor alpha mutant mice.2008
Author(s)
Nanno M, Kanari Y, Naito T, Inoue N, Hisamatsu T, Chinen H, Sugimoto K, Shimomura Y, Yamagishi H, Shiohara T, Ueha S, Matsushima K, Suematsu M, Mizoguchi A, Hibi T, Bhan AK, Ishikawa
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Journal Title
Gastroenterology 134(2)
Pages: 481-490
Related Report
Peer Reviewed
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[Journal Article] Non-pathogenic Escherichia coli strain Nissle 1917 inhibits signal transduction in intestinal epithelial cells.2008
Author(s)
Kamada N, Maeda K, Inoue N, Hisamatsu T, Okamoto S, Hong KS, Yamada T, Watanabe N, Tsuchimoto K, Ogata H, Hibi T
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Journal Title
Infect Immun 76(1)
Pages: 214-220
Related Report
Peer Reviewed
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[Journal Article] Imbalance in intestinal microflora constitution could be involved in the pathogenesis of inflammatory bowel disease.2008
Author(s)
Takaishi H, Matsuki T, Nakazawa A, Takada T, Kado S, Asahara T, Kamada N, Sakuraba A, Yajima T, Higuchi H, Inoue N, Ogata H, Iwao Y, Nomoto K, Tanaka R, Hibi T
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Journal Title
Int J Med Microbiol 298(5-6)
Pages: 463-472
Related Report
Peer Reviewed
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