Polysaccharides PS-G and Protein LZ-8 from Reishi (Ganoderma lucidum) Exhibit Diverse Functions in Regulating Murine Macrophages and T Lymphocytes
Polysaccharides PS-G and Protein LZ-8 from Reishi (Ganoderma lucidum) Exhibit Diverse Functions in Regulating Murine Macrophages and T Lymphocytes
复制标题
DOI：
10.1021/jf100914m
复制
发表时间：
2010-08-11
影响因子：
6.1
通讯作者：
Sheu, Fuu
中科院分区：
文献类型：
--
作者：
Yeh, Chen-Hao;Chen, Hsiao-Chin;Sheu, Fuu
灵芝中的生物活性成分主要包括多糖（PS-G）和免疫调节蛋白灵芝8（LZ-8）。这些成分可能在免疫系统中具有不同的调节功能。然而，不同工艺制备的PS-G制剂中仍含有部分LZ-8残留，表明PS-G和LZ-8的具体靶点和调节功能尚不完全清楚。在本研究中，PS-G 经过 15% TCA 去除蛋白质，使用抗 LZ-8 单克隆抗体进行 LZ-8 检测显示，去蛋白 PS-G (dpPS-G) 的蛋白质显着减少了 89.7%。产生表达未糖基化的重组LZ-8蛋白(rLZ-8)的酿酒酵母，然后与dpPS-G在对小鼠原代巨噬细胞和T淋巴细胞的诱导中进行比较。 TLR4缺陷型和野生型小鼠的腹膜巨噬细胞显示，TLR4是dpPS-G的假定受体，介导TNF-α、1L-1β和IL-12p70细胞因子的产生以及巨噬细胞上CD86、MHC II的表达，而rLZ-8通过另一种模糊途径增强IL-1β、IL-12p70、CD86和MHC II表达的产生。 rLZ-8处理的巨噬细胞增强了小鼠CD4(+)和CD8(+)T细胞释放的IFN-γ和IL-2，而dpPS-G处理没有增强IFN-γ和IL-2的释放。此外，虽然直接rLZ-8处理导致CD3(+) T细胞上显着的CD154、CD44表达，并增加CD4(+)和CD8(+) T细胞上IL-2、IFN-γ的分泌，但dpPS-G不能统一启动CD3(+)、CD4(+)或CD8(+) T细胞。总而言之，这些结果表明 LZ-8 可以激活小鼠巨噬细胞和 T 淋巴细胞，但 PS-G 只是巨噬细胞的激活剂，表明它们在激活先天性和适应性免疫中的不同作用。
Bioactive components in Ganoderma lucidum mainly include polysaccharides (PS-G) and immunomodulatory protein Ling Zhi-8 (LZ-8). These components may have diverse regulatory functions in the immune system. However, the PS-G preparations from different procedures still contained partial LZ-8 residue, indicating that the specific target and regulating function of PS-G and LZ-8 were not fully understood. In the present study, PS-G was subjected to 15% TCA for removing proteins and the LZ-8 detection using anti-LZ-8 monoclonal antibodies showed a remarkable 89.7% protein reduction of the deproteinized PS-G (dpPS-G). The Saccharomyces cerevisiae which expressed recombinant LZ-8 protein (rLZ-8) without glycosylation was generated and then compared with dpPS-G in the induction toward murine primary macrophage and T lymphocytic cells. The peritoneal macrophages from TLR4-deficient and wild type mice revealed that TLR4 was a putative receptor of dpPS-G, mediating the TNF-alpha, 1L-1 beta and IL-12p70 cytokine production and CD86, MHC II expression on macrophages, while rLZ-8 enhanced the production of IL-1 beta, IL-12p70, CD86, and MHC II expression by another obscure route. rLZ-8-treated macrophages enhanced the release of IFN-gamma and IL-2 by murine CD4(+) and CD8(+) T cells, whereas dpPS-G treatment did not enhance the release of IFN-gamma and IL-2. Furthermore, although the direct rLZ-8-treatment conduced dramatic CD154, CD44 expression on CD3(+) T cells and increased IL-2, IFN-gamma secretion on CD4(+) and CD8(+) T cells, the dpPS-G was incapable of priming CD3(+), CD4(+) or CD8(+) T cells unitarily. Taken together, these results demonstrated that LZ-8 could activate murine macrophages and T lymphocytes but PS-G was merely the activator for macrophages, suggesting their diverse roles in activating the innate and adaptive immunity.