1987 Fiscal Year Final Research Report Summary
Study on the synthesis, distribution and function of leukotrienes in the skin
| Project/Area Number |
61570490
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Dermatology
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| Research Institution | Kyoto University |
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Principal Investigator |
IKAI Kouichi Department of Dermatology Kyoto University Faculty of Medicine, 医学部, 講師 (00135568)
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| Co-Investigator(Kenkyū-buntansha) |
FURUKAWA Fukumi Department of Dermatology Kyoto University Faculty of Medicine, 医学部, 助手 (40156964)
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| Project Period (FY) |
1986 – 1987
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| Keywords | Skin / Arachidonic acid / Leukotrienes / Lipoxygenase / Immunihistochemistry / Radioimmunoassay Retinoids / アトピー性皮膚炎 / レチノイド |
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| Research Abstract |
Leukotrienes (LT) are potent biologically active compounds that are synthesized by the way of the lipoxygenase pathway in various tissues including the skin. L@tB4 is a potent chemotactic agent for neutrophils, and peptide-leukotrienes (LTC4, LTD4) contract respiratory, vascular, and intestinal smooth muscles. Although it has been reported that LTs play important roles in the pathogenesis of various skin diseases, including psoriasis and urticaria, the exact mechanism is not fully understood yet.
We examined the lipoxygenase activity in mouse skin. In mouse skin, the major lipoxygenase product was 12-HETE, followed by 15-HETE. A little amount of 5-HETE was also found. The HETE formation was inhibited by the addition of 5 <micrn>M AA-861. Ultraviolet light-B (500 mJ/cm^2) increased two-fold the formation of 12-HETE in mouse skin.
When arachidonic acid was topically applied to mouse ears, swelling of ears was observed. This response was inhibited by oral administration of vitamin A compounds (retinoids). The amount of LTB4 and peptide-leukotrienes, determined by radioimmunoassay, was also increased but suppressed by oral administered retinoids.
The biosynthesis of LTB4 by human polumorphonuclear leukocytes stimulated by A23187 was examined in the patients with atopic dermatitis and normal persons. There was no difference between patients and control on the production of LTB4.
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Research Products
(10 results)
