2011 Fiscal Year Final Research Report
Expression mechanism and pathological significance of Pentraxin 3 in macrophages and neutrophils.
Project/Area Number |
21590397
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Human pathology
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Research Institution | Niigata University |
Principal Investigator |
NAITO Makoto 新潟大学, 医歯学系, 教授 (30045786)
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Co-Investigator(Kenkyū-buntansha) |
OHASHI Riuko 新潟大学, 医歯学系, 助教 (20447600)
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Project Period (FY) |
2009 – 2011
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Keywords | マクロファージ / 好中球 / Pentraxin 3 / 潰瘍性大腸炎 |
Research Abstract |
Neutrophils in colonic mucosal tissue of patients with ulcerative colitis were main cellular source of Pentraxin 3(PTX3) protein, suggesting that PTX3 protein may contribute to cell-mediated immune defense in inflamed colon tissue of patients with ulcerative colitis. PTX3 protein was found to be present together with lactoferrin^+-specific granules localized in neutrophils. Upon IL-8 stimulation, PTX3 is released from PMNs and localized in Neutrophil Extracellular Traps(NETs) formed by extruded DNA. Macrophages showed granular positivity of PTX3. Secretion of PTX3 from stimulated neutrophils and macrophages was confirmed in culture. Binding of PTX3 on NETs appeared to be a defense mechanism against pathogens.
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Research Products
(10 results)
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[Journal Article] Long pentraxin 3(PTX3) expression and release by neutrophils in vitro and in ulcerative colitis2011
Author(s)
Savchenko AS, Inoue A, Ohashi R, Jiang S, Hasegawa G, Tanaka T, Hamakubo T, Kodama T, Aoyagi Y, Ushiki T, Naito M
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Journal Title
Pathol Int
Volume: 61
Pages: 290-297
Peer Reviewed
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[Journal Article] The proteomic profile of circulating pentraxin 3(PTX3) complex in sepsis demonstrates the interaction with azurocidin 1 and other components of neutrophil extracellular traps2011
Author(s)
Daigo K, Yamaguchi N, Kawamura T, Matsubara K, Jiang S, Ohashi R, Sudou Y, Kodama T, Naito M, Inoue K, Hamakubo T
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Journal Title
J Biol Chem
Volume: 286(1)
Pages: 674-86
Peer Reviewed
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