Ganoderma lucidum polysaccharides enhance CD14 endocytosis of LPS and promote TLR4 signal transduction of cytokine expression
Ganoderma lucidum polysaccharides enhance CD14 endocytosis of LPS and promote TLR4 signal transduction of cytokine expression
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DOI：
10.1002/jcp.21050
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发表时间：
2007-08-01
影响因子：
5.6
通讯作者：
Wong, Chi-Huey
中科院分区：
文献类型：
--
作者：
Hua, Kuo-Feng;Hsu, Hsien-Yeh;Wong, Chi-Huey
我们以前曾报道，一个良好的特征糖蛋白馏分含有岩藻糖残基的提取物中的灵芝多糖（EORP）发挥一定的免疫调节活性，通过刺激炎症细胞因子的表达，通过TLR 4。继续我们的研究，我们已经证明EORP增加小鼠巨噬细胞J774 A内CID 14和TLR 4的表面表达。I细胞，并进一步促进LPS结合和J774 A的摄取。I细胞以CID 14依赖的方式。此外，我们观察到共定位的内化LPS与溶酶体和高尔基体标记后5分钟内J774 A。用LPS刺激I细胞。此外，对J774 A. I细胞和人血液来源的原代巨噬细胞，随后LPS刺激，导致白细胞介素-I β（IL-1）表达的超诱导。内吞抑制剂：如细胞松弛素D和秋水仙碱有效地阻断J774 A对EORP增强的LPS内化。I细胞;然而，它们不能降低LPS诱导的某些促分裂原活化蛋白激酶的磷酸化，以及IL-1 mRNA和proIL-1蛋白表达，表明J774 A的LPS内化。I细胞与LPS依赖性激活无关。我们目前的研究结果可能提供了一个潜在的EORP相关的细菌感染的保护机制，通过增强IL-1的表达和清除污染的LPS的巨噬细胞。
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 CID 14 and TLR4 within murine macrophagesJ774A. I cells in vitro, and further promotes LPS binding and uptake by J774A. I cells in a CID 14-dependent fashion. Moreover, we observed the co-localization of internalized LPS with lysosome- and Golgi-apparatus markers within 5 min after J774A. I cells stimulated with LPS. In addition, EORP pretreatment of J774A. I cells and human blood-derived primary macrophages, followed by LPS stimulation, results in the super-induction of interleukin-I beta (IL-1) expression. Endocytosis inhibitors: such as cytochalasin D and colchicine effectively block EORP-enhanced LPS internalization byJ774A. I cells; yet they fail to decrease the LPS-induced phosphorylation of certain mitogen-activated protein kinases, and IL-I mRNA and proIL-1 protein expression, indicating that LPS internalization byJ774A. I 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.