| Project/Area Number |
09670874
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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 |
Dermatology
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| Research Institution | Hamamatsu University School of Medicine |
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Principal Investigator |
TOKUYA Yoshiki Hamamatsu University School of Medicine, 医学部・附属病院, 講師 (00172156)
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| Co-Investigator(Kenkyū-buntansha) |
WAKITA Hisashi 浜松医科大学, 医学部, 助手 (70242766)
FURUKAWA Fukumi 和歌山県立医科大学, 医学部, 教授 (40156964)
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| Project Period (FY) |
1997 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1999: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1998: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1997: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | superantigen / Staphylococcus / Keratinocyte / T cell / α-toxin / α-トキシン / 抗原提示細胞 |
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| Research Abstract |
Skin-colonization with Staphylococcus aureus (S. aureus) is one of the factors for exacerbartion of several skin disorders. It is suggested that this effect of S. aureus is mediated by activation of lesional T cells with released superantigens. Although T cells are effectively stimulated with staphylococcal superantigens in the presence of epidermal accessory cells, it remains to be elucidated whether in vivo cutaneous colonization with S. aureus can activate T cells. We examined how T cells are stimulated in the presence of keratinocytes by mitomycin C (MMC) -treated S. aureus that are unable to propagate but retain their ability to produce superantigens. Peripheral blood mononuclear cells (PBMC) proliferated well to MMC-treated, superantigen-producing S. aureus and bacterial supernatants. When purified T cells were cultured with MMC-treated S. aureus or supernatant in the presence of interferon-γ-pretreated keratinocytes, the supernatant, but not MMC-treated S. aureus, stimulated T cells. MMC-treated S. aureus had a cytotoxic effect on keratinocytes. Furthermore, keratinocytes were highly susceptible to α-toxin compared with monocytes and B cells functioning as accessory cells in PBMC. This suggests that no response of T cells to S. aureus plus keratinocytes is due to damage of superantigen-presenting function of keratinocytes by cytolysin. The activity of α-toxin was much less stable than that of superantigen during incubation. Given that S. aureus-colonized skin provides circumstances in which viable keratinocytes are exposed to excreted superantigens but not to active cytolysin(s), skin-infiltrating T cells may be effectively stimulated by S. aureus.
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