Bactericidal function of neutrophils in Crohn`s disease
Bactericidal function of neutrophils in Crohn`s disease
批准号:
22590708
负责人:
MATSUOKA Katsuyoshi
金额:
$2.91万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2010
资助国家:
日本
项目状态:
已结题
起止时间:
2010 至 2012
中文摘要
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英文摘要
The etiology of Crohn’s disease (CD), characterized by chronic intestinal inflammation, has not yet been identified. Interestingly, chronic granulomatous disease, in which neutrophil bactericidal function is impaired due the congenital defect of NADPH oxi1. Cytokine production2. Phagocytosis3.Reactive oxygen species (ROS) production4. Apoptosis, and6. Anti-microbial peptide (AMP) production. While no difference was observed in terms of apoptosis, phagocytosis, ROS production, or AMP production, neutrophils of CD patients produced significantly less IL-6 and IL-1 E compared with healthy controls. Fur
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DOI:
10.1111/j.1365-2567.2012.03554.x
发表时间:
2012-06-01
期刊:
IMMUNOLOGY
影响因子:
6.4
作者:
[Ichikawa, Riko, Takayama, Tetsuro, Hibi, Toshifumi]
通讯作者:
Hibi, Toshifumi
DOI:
10.1007/s00535-011-0425-7
发表时间:
2011-09-01
期刊:
JOURNAL OF GASTROENTEROLOGY
影响因子:
6.3
作者:
[Miyoshi, Jun, Yajima, Tomoharu, Hibi, Toshifumi]
通讯作者:
Hibi, Toshifumi
DOI:
10.1053/j.gastro.2012.07.108
发表时间:
2012-11-01
期刊:
GASTROENTEROLOGY
影响因子:
29.4
作者:
[Ono, Yuichi, Kanai, Takanori, Hibi, Toshifumi]
通讯作者:
Hibi, Toshifumi
Regulatory T Cells Suppress the Development of Colitis, Blocking Differentiation of T-helper 17 Into Alternative T-Helper 1 Cells.
调节性 T 细胞抑制结肠炎的发展,阻止辅助性 T 17 分化为替代性辅助性 T 细胞 1。
DOI:
--
发表时间:
2011
期刊:
Gastroenterology
影响因子:
29.4
作者:
[Sujino T, Kanai T, Ono Y, Mikami Y,Hayashi A, Doi T, Matsuoka K, HisamatsuT, Takaishi H, Ogata H, Yoshimura A,Littman DR, Hibi T.]
通讯作者:
Hibi T.
Mucosal CXCR4+ IgG plasma cells contribute to the pathogenesis of human ulcerative colitis through FcγR-mediated CD14 macrophage activation.
粘膜 CXCR4+ IgG 浆细胞通过 FcγR 介导的 CD14 巨噬细胞激活参与人类溃疡性结肠炎的发病机制。
DOI:
--
发表时间:
2012
期刊:
Gut
影响因子:
24.5
作者:
[Uo M, Hisamatsu T, Miyoshi J, Kaito D,Yoneno K, Kitazume MT, Mori M, Sugita A,Koganei K, Matsuoka K, Kanai T, Hibi T.]
通讯作者:
Hibi T.
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