...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Cellular Physiology >Ganoderma lucidum polysaccharides enhance CD14 endocytosis of LPS and promote TLR4 signal transduction of cytokine expression.
【24h】

Ganoderma lucidum polysaccharides enhance CD14 endocytosis of LPS and promote TLR4 signal transduction of cytokine expression.

机译：灵芝多糖增强CD14内吞作用的有限合伙人和促进TLR4信号转导的细胞因子表达。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

We have previously reported that a well-characterized glycoprotein fraction containing fucose residues in an extract of Ganoderma lucidum polysaccharides (EORP) exerts certain immuno-modulation activity by stimulating the expression of inflammatory cytokines via TLR4. Continuing our studies, we have demonstrated that EORP increases the surface expression of CD14 and TLR4 within murine macrophages J774A.1 cells in vitro, and further promotes LPS binding and uptake by J774A.1 cells in a CD14-dependent fashion. Moreover, we observed the co-localization of internalized LPS with lysosome- and Golgi-apparatus markers within 5 min after J774A.1 cells stimulated with LPS. In addition, EORP pretreatment of J774A.1 cells and human blood-derived primary macrophages, followed by LPS stimulation, results in the super-induction of interleukin-1beta (IL-1) expression. Endocytosis inhibitors: such as cytochalasin D and colchicine effectively block EORP-enhanced LPS internalization by J774A.1 cells; yet they fail to decrease the LPS-induced phosphorylation of certain mitogen-activated protein kinases, and IL-1 mRNA and proIL-1 protein expression, indicating that LPS internalization by J774A.1 cells is not associated with LPS-dependent activation. Our current results could provide a potential EORP-associated protection mechanism for bacteria infection by enhancing IL-1 expression and the clearance of contaminated LPS by macrophages.
机译：我们以前报道,良好的糖蛋白分数含有植物提取的残留灵芝多糖(EORP)产生通过刺激某些immuno-modulation活动炎性细胞因子的表达TLR4。证明EORP增加了表面在小鼠CD14和TLR4的表达巨噬细胞J774A。促进有限合伙人J774A绑定和吸收。CD14-dependent时尚。观察了内化的有限合伙人与溶酶体和高尔基体标记内J774A后5分钟。此外,J774A EORP预处理。人类血液的主要巨噬细胞,紧随其后LPS刺激的结果super-induction interleukin-1beta (il - 1)表达式。细胞松弛素D和秋水仙碱有效地阻止J774A.1 EORP-enhanced有限合伙人内化细胞;磷酸化的增殖作用蛋白激酶,il - 1 mRNA和proIL-1蛋白表达,表明有限合伙人由J774A内化。与LPS-dependent激活有关。目前可以提供一个潜在的结果EORP-associated细菌的保护机制通过增强il - 1的表达和感染通过巨噬细胞清除污染的有限合伙人。

著录项

相似文献

  • 外文文献
  • 中文文献
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号