腸管細胞株HT-29におけるヒトミルクオリゴ糖のToll様受容体2，4およびMD2遺伝子発現に及ぼす影響

DOI 機関リポジトリ 日本農学文献記事索引 Web Site Web Site 参考文献72件
  • 朝隈 貞樹
    農業・食品産業技術総合研究機構北海道農業研究センター集約放牧研究チーム
  • 横山 朋子
    帯広畜産大学食品科学研究部門畜産食品科学ユニット
  • 木村 一雅
    ヤクルト中央研究所
  • 渡邊 陽子
    ヤクルト中央研究所
  • 中村 正
    帯広畜産大学食品科学研究部門畜産食品科学ユニット
  • 福田 健二
    帯広畜産大学大学院畜産学研究科食品衛生学講座
  • 浦島 匡
    帯広畜産大学大学院畜産学研究科食品衛生学講座

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タイトル別名
  • Effect of Human Milk Oligosaccharides on Messenger Ribonucleic Acid Expression of Toll-like Receptor 2 and 4, and of MD2 in the Intestinal Cell Line HT-29

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It is believed that human milk oligosaccharides (HMO) act as receptor analogues that inhibit the attachment of pathogenic microorganisms to the infant colon, but the direct involvement of HMO in anti infection has not as yet been demonstrated. The present study was conducted to clarify whether HMOs as well as commercially available galacto oligosaccharides (GO), from which lactose has been removed, affect the expression of toll-like receptor (TLR) 2 and 4, and of MD2 mRNA in the HT-29, human colonic cell line. HT-29 cells were treated with neutral human milk oligosaccharides (nHMOs), which had been separated from the acidic oligosaccharide fraction and also from lactose, as well as with GOs. HT-29 cells were treated with specific oligosaccharides of major components of nHMO or GO. The mRNA expression of TLR2, 4 and MD2 were measured using Real-time RT-PCR normalized to glyceraldehydes 3-phosphate dehydrogenase (GAPDH) mRNA expression. The addition of nHMO affected the expression of TLR2. Treatment with 1.0 mg/mL of nHMO as well as with 0.5 mg and 1.0 mg/mL GO enhanced the mRNA expression of TLR4. In experiments with specific oligosaccharides, treatments with 3'-sialyllactose (3'-SL), 6'-sialyllactose (6'-SL) or 6'-galactosyllactose (6'-GL) increased the expression of TLR-2, while the administration of lacto-N-fucopentaose I (LNFP I), 3'-, 6'-SL or 6'-GL enhanced that of TLR4. These results suggest that HMOs as well as GOs had a direct effect on colonic epithelial cells, with induction of the mRNA expression of TLR.

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