| Project/Area Number |
26461703
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Dermatology
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| Research Institution | Juntendo University |
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Principal Investigator |
NIYONSABA Francois 順天堂大学, 医学(系)研究科(研究院), 先任准教授 (60365640)
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| Research Collaborator |
AKIYAMA Toshihiro
KIATSURAYANON Chanisa
UMEHARA Yoshie
SMITHRITHEE Rithee
IKEDA Shigaku
OKUMURA Ko
OGAWA Hideoki
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | ケラチノサイト / 抗菌物質 / タイトジャンクション / 皮膚免疫 / アトピー性皮膚炎 / 痒み / 炎症 / 抗菌ペプチド |
|---|
| Outline of Final Research Achievements |
In this study, we evaluated the effects of LL-37 on regulation of keratinocyte tight junction (TJ) barrier function. We found that LL-37 increased the expression of TJ proteins and keratinocyte differentiation markers, and markedly strengthened the TJ barrier function via Rac1, atypical protein kinase C, glycogen synthase kinase-3 and PI3 kinase pathways. Similar to LL-37, humanβ-defensin-3 also enhanced the TJ barrier function. In addition, LL-37 induced the expression of semaphorin 3A, an itch inhibitor, implying LL-37 possible application to pruritus. Taken together, our findings that LL-37 andβ-defensin-3 enhance TJ barrier function, inhibit itch and inflammation suggest the potential use of skin-derived antimicrobial peptides for the understanding atopic dermatitis pathological mechanism and treatment.
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