Role of Eosinophils in Hepatic Ischemia Reperfusion Injury

嗜酸性粒细胞在肝缺血再灌注损伤中的作用

基本信息

  • 批准号:
    10365939
  • 负责人:
  • 金额:
    $ 38.83万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2019
  • 资助国家:
    美国
  • 起止时间:
    2019-06-01 至 2023-04-30
  • 项目状态:
    已结题

项目摘要

PROJECT SUMMARY The goal of this proposal is to investigate the functional role of eosinophils during hepatic ischemia and reperfusion injury (IRI). Hepatic IRI is a significant source of morbidity and mortality during major hepatic resection and during liver transplantation. Previous studies have shown that following liver transplantation innate immune cells, such as neutrophils or macrophages, are activated and traffic into the hepatic allograft. Unexpectedly, we observed that eosinophils also accumulate in the liver following orthotopic liver transplantation in humans. In contrast, we could not detect any eosinophils in healthy liver biopsies. Similarly, in a murine model, eosinophils accumulate in the liver in a time-dependent fashion following hepatic IRI. Functional studies using genetic and antibody-based depletion of eosinophils demonstrate a protective role of these cells during hepatic IRI. An unbiased screen of gene expression profiles following eosinophil depletion implicated eosinophil-dependent ST2 in liver protection. Combination of genetic and adoptive transfer studies suggest that eosinophil-specific IL-33/ST2 signaling attenuates inflammation of the ischemic liver by dampening hepatic neutrophil accumulation/activation. These findings led to our hypothesis that during hepatic IRI, eosinophils protect the liver through IL-33/ST2 signaling. Three Specific Aims are proposed to i) investigate the role of eosinophils and IL-33/ST2 signaling in hepatic IRI, ii) elucidate the mechanism by which IL-33/ST2 signaling in eosinophils protects against hepatic IRI, and iii) Target IL-33/ST2 signaling in eosinophils for the treatment of hepatic IRI.
项目总结

项目成果

期刊论文数量(0)
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会议论文数量(0)
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Cynthia Ju其他文献

Cynthia Ju的其他文献

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{{ truncateString('Cynthia Ju', 18)}}的其他基金

Role of neutrophil-specific NOX2 in alcohol-induced liver injury
中性粒细胞特异性NOX2在酒精性肝损伤中的作用
  • 批准号:
    10621545
  • 财政年份:
    2023
  • 资助金额:
    $ 38.83万
  • 项目类别:
Role of chitinase-3-like-1 (Chi3l1) in acetaminophen-induced liver injury
几丁质酶 3-like-1 (Chi3l1) 在对乙酰氨基酚诱导的肝损伤中的作用
  • 批准号:
    10674986
  • 财政年份:
    2019
  • 资助金额:
    $ 38.83万
  • 项目类别:
Role of chitinase-3-like-1 (Chi3l1) in acetaminophen-induced liver injury
几丁质酶 3-like-1 (Chi3l1) 在对乙酰氨基酚诱导的肝损伤中的作用
  • 批准号:
    9898894
  • 财政年份:
    2019
  • 资助金额:
    $ 38.83万
  • 项目类别:
Role of chitinase-3-like-1 (Chi3l1) in acetaminophen-induced liver injury
几丁质酶 3-like-1 (Chi3l1) 在对乙酰氨基酚诱导的肝损伤中的作用
  • 批准号:
    10464890
  • 财政年份:
    2019
  • 资助金额:
    $ 38.83万
  • 项目类别:
Role of Eosinophils in Hepatic Ischemia Reperfusion Injury
嗜酸性粒细胞在肝缺血再灌注损伤中的作用
  • 批准号:
    10658011
  • 财政年份:
    2019
  • 资助金额:
    $ 38.83万
  • 项目类别:
Role of chitinase-3-like-1 (Chi3l1) in acetaminophen-induced liver injury
几丁质酶 3-like-1 (Chi3l1) 在对乙酰氨基酚诱导的肝损伤中的作用
  • 批准号:
    10019530
  • 财政年份:
    2019
  • 资助金额:
    $ 38.83万
  • 项目类别:
Role of chitinase-3-like-1 (Chi3l1) in acetaminophen-induced liver injury
几丁质酶 3-like-1 (Chi3l1) 在对乙酰氨基酚诱导的肝损伤中的作用
  • 批准号:
    10219240
  • 财政年份:
    2019
  • 资助金额:
    $ 38.83万
  • 项目类别:
Role of gp91phox in Hepatic MF Programming and Alcohol Liver Disease
gp91phox 在肝脏 MF 编程和酒精性肝病中的作用
  • 批准号:
    9129373
  • 财政年份:
    2016
  • 资助金额:
    $ 38.83万
  • 项目类别:
Effect of Lactoferrin on Alcohol-Induced Dysbiosis and Gut Barrier Dysfunction
乳铁蛋白对酒精引起的生态失调和肠道屏障功能障碍的影响
  • 批准号:
    8738543
  • 财政年份:
    2013
  • 资助金额:
    $ 38.83万
  • 项目类别:
Effect of Lactoferrin on Alcohol-Induced Dysbiosis and Gut Barrier Dysfunction
乳铁蛋白对酒精引起的生态失调和肠道屏障功能障碍的影响
  • 批准号:
    8568645
  • 财政年份:
    2013
  • 资助金额:
    $ 38.83万
  • 项目类别:

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ATTAC 时间:针对 gp100 细胞的 T 细胞过继转移来治疗 LAM
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