The nutritional supplement Active Hexose Correlated Compound (AHCC) has direct immunomodulatory actions on intestinal epithelial cells and macrophages involving TLR/MyD88 and NF-κB/MAPK activation

The nutritional supplement Active Hexose Correlated Compound (AHCC) has direct immunomodulatory actions on intestinal epithelial cells and macrophages involving TLR/MyD88 and NF-κB/MAPK activation
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DOI:
10.1016/j.foodchem.2012.09.039
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发表时间:
2013-02-01
期刊:
影响因子:
8.8
通讯作者:
Martinez-Augustin, Olga
Martinez-Augustin, Olga
中科院分区:
农林科学1区
文献类型:
--
作者:
Daddaoua, Abdelali;Martinez-PIata, Enrique;Martinez-Augustin, Olga

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活性己糖相关化合物 (AHCC) 是一种免疫刺激营养补充剂。 AHCC 对肠上皮细胞或单核细胞的影响和作用机制的描述很少。将AHCC添加到肠上皮细胞(IEC18和HT29细胞)和单核细胞(THP-1细胞)的培养基中,并通过ELISA评估促炎细胞因子的分泌。使用 NF kappa B 和 MAPK 抑制剂来研究信号转导途径,同时使用 shRNA 在 IEC18 细胞中沉默 TLR4 和 MyD88。研究发现,AHCC 诱导 HT29 细胞 IEC18 和 IL-8 中 GRO α 和 MCP1 的分泌。这些作用取决于 NF kappa B 激活,部分取决于 MAPK 激活以及 MyD88 和 TLR4 的存在。在 THP-1 细胞中,AHCC 诱发 IL-8、IL-1 β 和 TNF-α 分泌。 IL-8 的诱导依赖于 JNK 和 NF kappa B 的激活。因此,AHCC对肠上皮细胞和单核细胞发挥免疫刺激作用涉及TLR4/MyD88和NF kappa B/MAPK信号转导通路。 (C) 2012 Elsevier Ltd. 保留所有权利。
Active Hexose Correlated Compound (AHCC) is an immunostimulatory nutritional supplement. AHCC effects and mechanism of action on intestinal epithelial cells or monocytes are poorly described. AHCC was added to the culture medium of intestinal epithelial cells (IEC18 and HT29 cells) and monocytes (THP-1 cells) and assessed the secretion of proinflammatory cytokines by ELISA. Inhibitors of NF kappa B and MAPKs were used to study signal transduction pathways while TLR4 and MyD88 were silenced in IEC18 cells using shRNA. It was found that AHCC induced GRO alpha and MCP1 secretion in IEC18 and IL-8 in HT29 cells. These effects depended on NF kappa B activation, and partly on MAPKs activation and on the presence of MyD88 and TLR4. In THP-1 cells AHCC evoked IL-8, IL-1 beta and TNF-alpha secretion. The induction of IL-8 depended on JNK and NF kappa B activation. Therefore, AHCC exerts immunostimulatory effects on intestinal epithelial cells and monocytes involving TLR4/MyD88 and NF kappa B/MAPK signal transduction pathways. (C) 2012 Elsevier Ltd. All rights reserved.