| Project/Area Number |
14570507
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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 | Keio University |
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Principal Investigator |
NAGATA Hiroshi KEIO UNIVERSITY, MEDICINE, ASSOCIATE PROFESSOR, 医学部, 助教授 (00146599)
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| Co-Investigator(Kenkyū-buntansha) |
SUZUKI Hidekazu KEIO UNIVERSITY, MEDICINE, ASSISTANT PROFESSOR, 医学部, 講師 (70255454)
SUEMATSU Makoto KEIO UNIVERSITY, MEDICINE, PROFESSOR, 医学部, 教授 (00206385)
MINAMITANI Haruyuki KEIO UNIVERSITY, SCIENCE AND TECHNOLOGY, PROFESSOR, 医学部, 教授 (70051779)
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| Project Period (FY) |
2002 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2004: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2003: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2002: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Keywords | macrophage / dendritic cell / colitis / lymphatic vessel in mesentery / mesenteric lymph node / chemokine / リンパ球ホーミング |
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| Research Abstract |
Regulation of lymphocyte migration in the intestine under physiological and pathological condition
TECK/CCL25 plays an important role in the adherence of mucosal lymphocytes to the small intestine but not the colon under uniflamed as well as inflamed conditions. CD4T lymphocytes significantly accumulated in villus as well as in Peyer' s patches via a MAdCAM-1-dependent process in rats with a chronic allergy to ovalbumin.
Migration kinetics of dendritic cells via intestinal lymph
The isolated dendritic cells accumulated in mesenteric lymph nodes in a time-dependent manner with maximal accumulation at 48 h. Inhibition of ICAM-1 or CD11b/c did not affect DC migration. The migratory ability of dendritic cells correlates well with their degree of maturation, and different chemokine/chemokine receptor usage may be the main regulator of dendritic cell migration kinetics through intestinal lymph.
Response of macrophage in mesenteric lymph node
Parasinus macrophages play a role in the transient anti-metastatic capability of the node, and cytokines secreted by these cells increased at the early stages of metastasis. Deterioration of cytokine induction may be responsible for subsequent cancer proliferation. Macrophage migration inhibitory factor expressed in the cancer cells may modulate cytokine responses and migration of the macrophages.
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