| Project/Area Number |
15K21370
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Dermatology
Pharmacology in pharmacy
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| Research Institution | Keio University |
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Principal Investigator |
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| Research Collaborator |
TSUJI Shoutaro
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 乾癬 / SLURP-1 / 黄色ブドウ球菌 / 抗菌活性 / 皮膚バリア機能 / 正常ヒト表皮角化細胞 / α7ニコチン性アセチルコリン受容体 / T-reg / IL-22 |
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| Outline of Final Research Achievements |
SLURP1 is the causal gene for Mal de Meleda (MDM), an autosomal recessive skin disorder characterized by diffuse palmoplantar keratoderma and transgressive keratosis. Recently, SLURP1-deficient mice show MDM-like symptoms such as severe palmoplantar keratoderma characterized by increased keratinocyte proliferation and water barrier defects. Although SLURP1 likely serves as an important proliferation/differentiation factor in keratinocytes, the possible relation between SLURP1 and other skin diseases, such as psoriasis and atopic dermatitis, has not been studied. In our experiment, we found SLURP1 expression is greatly increased within the skin lesions in a psoriatic mouse model. In addition, recombinant SLURP1 suppressed the growth of S. aureus, which is associated with disease severity in psoriasis. These results suggest that SLURP1 may contribute to the pathogenesis of psoriasis.
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