1999 Fiscal Year Final Research Report Summary
Crosstalk of immune and nervous systems by 3-D imaging
| Project/Area Number |
10044312
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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 |
Physical pharmacy
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| Research Institution | Nagoya City University |
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Principal Investigator |
NAKANISHI Mamoru Nagoya City University Faculty of Pharmaceutical Sciences Professor, 薬学部, 教授 (90090472)
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| Co-Investigator(Kenkyū-buntansha) |
TESHIMA Reiko National Institute of Health Sciences Principal Investigator, 主任研究官 (50132882)
FURUNO Tadahide Nagoya City University Faculty of Pharmaceutical Sciences Assistant Professor, 薬学部, 講師 (80254308)
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| Project Period (FY) |
1998 – 1999
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| Keywords | Allergy / Mast cells / Bradykinin / Confocal laser scanning microscopy / Calcium ion / NK-1 antagonist / Substance P / Nerves |
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| Research Abstract |
Communication between nerves and mast cells is a prototypic demonstration of neuroimmune interaction. However, whether mast cell activation occurs as a direct response to neuronal activation or requires an intermediary cell is unclear. Addressing this issue, we used an in vitro coculture approach comprising cultured murine superior cervical ganglia and rat leukemia basophilic cells (RBLs ; possesses properties of mucosal-type mast cells). Following loading with the calcium fluorophore, Fluo-3, neurite-RBL units (separated by <50nm) were examined by confocal laser scanning microscopy. Addition of bradykinin, or scorpion venom, dose-dependently elicited neurite activation (i.e., CaィイD12+ィエD1 mobilization) and, after a lag period, RBL CaィイD12+ィエD1 mobilization. Neither bradykinin nor scorpion venom had any direct effect on the RBLs in the absence of neurites. Addition of a neutralizing substance P Ab or a neurokinin (NK)-1 receptor antagonist, but not an NK-2 receptor antagonist, dose-dependently prevented the RBL activation that resulted as a consequence of neural activation by either bradykinin or scorpion venom. These data illustrate that nerve-mast cell cross-talk can occur in the absence of an intermediary transducing cell and that the neuropeptide substance P, operating via NK-1 receptors, is an important mediator of this communication. Our findings have implications for the neuroimmune signaling cascades that are likely to occur during airways inflammation, intestinal hypersensitivity, and other conditions in which mast cells feature.
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