| Project/Area Number |
24591461
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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 |
膠原病・アレルギー・感染症内科学
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| Research Institution | Keio University (2013-2014)
The University of Tokyo (2012) |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
URANO Yasuteru 東京大学, 大学院医学系研究科 生体物理医学専攻医用生体工学講座 生体情報学分野, 教授 (20292956)
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| Research Collaborator |
OKUBO Koshu 慶應義塾大学, 医学部, 助教 (60749125)
KAMIYA Mako 東京大学, 大学院医学系研究科 生体物理医学専攻, 助教 (90596462)
KAWAKAMI Hiroshi 共立女子大学, 家政学部, 教授 (90458860)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | neutrophil / inflammation / lactoferrin / autoimmune / vasculitis / 好中球 / 好中球細胞外トラップ / ラクトフェリン / 炎症 / 自己免疫 / 血管炎 / 腎炎 / NETｓ / 血栓 |
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| Outline of Final Research Achievements |
Neutrophil extracellular traps (NETs) are associated with the development of autoimmune and/or inflammatory diseases. We found that lactoferrin translocates from the cytoplasm to the plasma membrane of neutrophils upon stimulation and strongly suppresses NETs without effects on oxygen radicals generation. Exogenous lactoferrin significantly shrunk the chromatin fibers in the released NETs. The results that lactoferrin removed positive charge failed to inhibit NET formation suggested that charge-charge interaction between lactoferrin and NETs are required in the function. Lactoferrin suppressed development of autoimmune small-vessel vasculitis and NETs release into the circulation. These observations suggest that lactoferrin serves as an intrinsic inhibitor of NETs and subsequent DNA release into the circulation. Taken together, our data indicate that lactoferrin may represent a therapeutic lead for controlling NET release in autoimmune and/or inflammatory diseases.
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