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Dynamic Function of Peritoneal Exudative Neutrophils As a Defense Mechanism in Acute Pancreatitis

Dynamic Function of Peritoneal Exudative Neutrophils As a Defense Mechanism in Acute Pancreatitis
腹腔渗出性中性粒细胞作为急性胰腺炎防御机制的动态功能
批准号:
15591441
负责人:
SUGIYAMA Masanori
金额:
$2.05万
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:
2003
资助国家:
日本
项目状态:
已结题
起止时间:
2003 至 2005

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中文摘要
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英文摘要
Acute necrotizing pancreatitis is often complicated by pancreatic or peripancreatic infection. Since necrotizing pancreatitis may impair immune function, thereby increasing susceptibility to bacterial infection, we examined the expression of surface opsonin receptors (CD11b, complement receptor 3; CD32/CD16, immunoglobulin GFc receptor) on local neutrophils in murine acute pancreatitis. The necrotizing and edematous forms of acute pancreatitis were induced by seven subcutaneous injections of caerulein with and without intraperitoneal administration of lipopolysaccharide, respectively. Peritoneal exudative neutrophils were counted and assayed for receptor expression by flow cytometry, serially, from 1 to 24 hours after induction of pancreatitis. The peritoneal exudative neutrophil count was greater inedematous than in necrotizing pancreatitis. The number of CD 11b-positive peritoneal exudative neutrophils was elevated in edematous pancreatitis, but the number was lower in necrotizing than in edematous pancreatitis at 6-24 hours. The mean fluorescence intensity of CD11b on neutrophils was comparable in both pancreatitis models. The cell count and mean fluorescence intensity indicated upregulated expression of CD32/CD16 on peritoneal exudative neutrophils in edematous pancreatitis, whereas the upregulation was attenuated in necrotizing pancreatitis. In conclusion, opsonin receptor expression on local neutrophils was reduced in necrotizing pancreatitis, compared to edematous pancreatitis, and the difference may be responsible for the local septic complications in necrotizing pancreatitis.
期刊论文(4)
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会议论文
Acute necrotizing pancreatitis reduces opsonin receptor expression on peritoneal exudative neutrophils in mice.
急性坏死性胰腺炎降低小鼠腹膜渗出性中性粒细胞的调理素受体表达。
DOI: --
发表时间: 2005
期刊: Hepatogastroenterology 52
影响因子: --
作者: [Sugiyama M, Hatano N, Watanabe T, Atomi Y]
通讯作者: Atomi Y
Acute necrotizing pancreatitis reduces opsonin receptor expression on peritoneal exudative neutrophils in mice
急性坏死性胰腺炎降低小鼠腹膜渗出性中性粒细胞调理素受体表达
DOI: --
发表时间: 2005
期刊: Hepatogastroenterology 52・65
影响因子: --
作者: [Sugiyama M, Hatano N, Watanabe T, Atomi Y]
通讯作者: Atomi Y
A molecular mechanism for copper transportation to tyrosinase that is assisted by a metallochaperone, caddie protein
  • 批准号:
    22550153
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 资助金额:
    $3.08万
  • 财政年份:
    2010
  • 负责人:
    SUGIYAMA Masanori
  • 依托单位:
Opsonin Receptor Expression on Peritoneal Exudative and Circulatory Neutrophils in Murine Acute Pancreatitis
  • 批准号:
    13671335
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 资助金额:
    $1.98万
  • 财政年份:
    2001
  • 负责人:
    SUGIYAMA Masanori
  • 依托单位:
Effects of chronic pancreatic impairment on development of acute pancreatitis
  • 批准号:
    11671270
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 资助金额:
    $1.54万
  • 财政年份:
    1999
  • 负责人:
    SUGIYAMA Masanori
  • 依托单位:
Immunohistochemical localization of beta1,4-galactosyltransferase in human normal and neoplastic pancreatic tissues
  • 批准号:
    09671335
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 资助金额:
    $1.15万
  • 财政年份:
    1997
  • 负责人:
    SUGIYAMA Masanori
  • 依托单位:
海外基金