| Project/Area Number |
17390310
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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 |
Dermatology
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| Research Institution | University of Yamanashi |
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Principal Investigator |
SHIMADA Shinji University of Yamanashi, Department of Research Interdisciplinary Graduate School of Medicine and Engineering, Professor, 大学院医学工学総合研究部, 教授 (10114505)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUE Hiroyuki Chiba University, Graduate School of Medicine, Professor, 医学(系)研究科(研究院), 教授 (10250424)
SHIBAGAKI Naotaka University of Yamanashi, Department of Research Interdisciplinary Graduate School of Medicine and Engineering, Associate Professor, 大学院医学工学総合研究部, 助教授 (40262662)
NAGASAKA Akiko University of Yamanashi, University of Yamanashi Hospital, Resiearch Associafe, 大学院医学部附属病院, 助手 (60377546)
AOKI Rui University of Yamanashi, University of Yamanashi Hospital, Instructor, 大学院医学部附属病, 医員 (10377541)
NISHIYAMA Hiroyuki Nagoya University, School of Medicine, Professor, 大学院医学系研究科, 教授 (60115615)
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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 |
¥15,300,000 (Direct Cost: ¥15,300,000)
Fiscal Year 2006: ¥7,400,000 (Direct Cost: ¥7,400,000)
Fiscal Year 2005: ¥7,900,000 (Direct Cost: ¥7,900,000)
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| Keywords | Mast cell / Herpes simplex virus / Toll-like receptor / Innate immunity / Acquired immunity |
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| Research Abstract |
Mast cells have long been considered as major effector cells in type I-allergic responses. Recent studies, however, have revealed the additional importance of mast cells in host defense against pathogens, especially bacteria. Although we have recently reported that cutaneous mast cells express functional Toll-like receptors (TLRs) that recognize viral components, it remains largely unknown whether mast cells are involved in host defense against viruses. We hypothesized that degranulation and inflammatory cytokine production by mast cells may be induced upon herpes simplex virus (HSV) infection, thus being involved in the inflammatory and immune responses against the virus. To test this, we used murine fetal skin-derived cultured mast cells (FSMC). Rapid (within 10 min) degranulation by FSMC was induced in a virus number-dependent fashion without affecting cell viability, when HSVwas added to FSMC cultures (β-hexosaminidase assay). The viral components were detected within 24 h after the infection (immunohistochemistry). In addition, inflammatory cytokines (i.e., TNFα, IL-6, and IFNβ) were not induced in the culture supernatants 24 h post infection. Upon inoculation of HSV (5 x 10^5 PFU) intradermally into BALB/c mice, the dermal infiltrates and significant increase in the number of degranulated mast cells were observed within 2 h (toluidine blue staining). These results indicate that cutaneous mast cells degranulate without elaborating inflammatory cytokines upon HSV infection, thus participating in the induction of inflammatory responses and the subsequent acquired immune responses against the virus.
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