Role of intraperitoneal cell-traffic and TGF superfamily members in inflammatory bowel diseases
| Project/Area Number |
17590693
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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 | Research Institute, International Medical Center of Japan |
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Principal Investigator |
DOHI Taeko Research Insitute, International Medial Center of Japan, Department of Gastroenterology, Director, 消火器疾患研究部, 部長 (60250221)
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| Co-Investigator(Kenkyū-buntansha) |
TOYAMA Noriko (SORIMACHI Noriko) Research Insitute, International Medial Center of Japan, Division head, 消火器疾患研究部, 室長 (30217468)
MIZUTANI Noriko Research Insitute, International Medial Center of Japan, Research fellow, 消火器疾患研究部, 流動研究員 (00392390)
KAWASHIMA Rei Research Insitute, International Medial Center of Japan, Research fellow, 消火器疾患研究部, 流動研究員 (70392389)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2005: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | Inflammatory bowel disease / Macrophages / chemokines / Mesothelial cells / 炎症件腸疾患 / 腹腔マクロファージ / マウス腸炎モデル |
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| Research Abstract |
The aim of this study was to clarify the mechanism of inflammatory cell infiltration in mouse model of inflammatory bowel disease by focusing the cell trafficking and immune system in the peritoneal cavity. Initially we found great loss of peritoneal macrophages in peritoneal exudate after induction of colitis and increased number of immature granulocyte-type cells. We investigated the specific recruitment of peritoneal macrophages (PMФs) by adoptive transfer of fluorescence-labeled peritoneal macrophages, and their expression of chemokine receptors. PMФs aggregated at the site of injured serosal side of the colon. The chemokine receptor CCR8 was upregulated in the aggregating PMФs when compared with naive PMФs. The upregulation of CCR8 was also observed in PMФs, but not in bone marrow-derived macrophages, treated with inflammatory stimulants including bacterial components and cytokines. Importantly, CCL1, the ligand for CCR8, a product of both PMФs and peritoneal mesothelial cells (PMCs) following inflammatory stimulation, was a potent enhancer of CCR8 expression. LPS-challenged PMФs also produced a TGF-superfamily member activin. Cell aggregation involving PMФand PMCs was induced in vitro in the presence of CCL1. CCR8 gene deficient mice or mice treated with anti-CCL1 neutralizing antibody exhibited significantly reduced serosal macrophage accumulation. Our study now establishes a unique autocrine activation system in PMФ and the mechanism for recruitment of PMФs together with PMCs via CCL1/CCR8, as immune responses of peritoneal cavity. Here we found an efficient defense mechanism as a specific function of peritoneal macrophages when inflammatory or surgical stress reaches to the deep inside of the body.
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Report
(3 results)
Research Products
(28 results)
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Author(s)
Kunisaki R, Ikawa S, Maeda T, Nakazaki Y, Kurita R, Harata M, Shutoh Y, Bai Y, Soda Y, Tanabe T, Dohi T, Kato R, Ikawa Y, Sekihara H, Asano S, Tani K
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Journal Title
J. Gene Med. 8
Pages: 1121-1130
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Journal Title
J Immunol 177
Pages: 3045-3054
Description
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