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GPR31-dependent dendrite protrusion of intestinal CX3CR1~+ cells by bacterial metabolites

机译：细菌代谢产物对肠CX3CR1〜+细胞的GPR31依赖性树突突起

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摘要

Small intestinal mononuclear cells that express CX3CR1 (CX3CR1(+) cells) regulate immune responses(1-5). CX3CR1(+) cells take up luminal antigens by protruding their dendrites into the lumen(1-4,6). However, it remains unclear how dendrite protrusion by CX3CR1(+) cells is induced in the intestine. Here we show in mice that the bacterial metabolites pyruvic acid and lactic acid induce dendrite protrusion via GPR31 in CX3CR1(+) cells. Mice that lack GPR31, which was highly and selectively expressed in intestinal CX3CR1(+) cells, showed defective dendrite protrusions of CX3CR1(+) cells in the small intestine. A methanol-soluble fraction of the small intestinal contents of specific-pathogen-free mice, but not germ-free mice, induced dendrite extension of intestinal CX3CR1(+) cells in vitro. We purified a GPR31-activating fraction, and identified lactic acid. Both lactic acid and pyruvic acid induced dendrite extension of CX3CR1(+) cells of wild-type mice, but not of Gpr31b(-/-) mice. Oral administration of lactate and pyruvate enhanced dendrite protrusion of CX3CR1(+) cells in the small intestine of wild-type mice, but not in that of Gpr31b(-/-) mice. Furthermore, wild-type mice treated with lactate or pyruvate showed an enhanced immune response and high resistance to intestinal Salmonella infection. These findings demonstrate that lactate and pyruvate, which are produced in the intestinal lumen in a bacteria-dependent manner, contribute to enhanced immune responses by inducing GPR31-mediated dendrite protrusion of intestinal CX3CR1(+) cells.
机译：表达CX3CR1的小肠单核细胞（CX3CR1（+）细胞）调节免疫反应（1-5）。 CX3CR1（+）细胞通过将树突突入管腔来吸收腔内抗原（1-4,6）。但是，尚不清楚如何在肠道中诱导CX3CR1（+）细胞的树突突出。在这里，我们在小鼠中显示细菌代谢物丙酮酸和乳酸通过CX3CR1（+）细胞中的GPR31诱导枝晶突出。缺乏GPR31的小鼠在肠道CX3CR1（+）细胞中高度选择性表达，在小肠中显示CX3CR1（+）细胞的树突突起缺陷。不含特定病原体的小鼠（而非无菌小鼠）的小肠内容物的甲醇可溶部分在体外诱导肠CX3CR1（+）细胞的树突扩展。我们纯化了GPR31活化级分，并鉴定了乳酸。乳酸和丙酮酸都可以诱导野生型小鼠CX3CR1（+）细胞的树突扩展，而不是Gpr31b（-/-）小鼠。口服乳酸和丙酮酸可增强野生型小鼠小肠中CX3CR1（+）细胞的树突突起，但不适用于Gpr31b（-/-）小鼠。此外，用乳酸或丙酮酸处理的野生型小鼠显示出增强的免疫反应和对肠沙门氏菌感染的高抗性。这些发现表明，以细菌依赖性方式在肠腔中产生的乳酸和丙酮酸通过诱导GPR31介导的肠CX3CR1（+）细胞的树突突出而有助于增强免疫反应。

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  • 来源
    《Nature》 |2019年第7742期|110-114|共5页
  • 作者

    Morita Naoki; Umemoto Eiji; Fujita Setsuko; Hayashi Akio; Kikuta Junichi; Kimura Ikuo; Haneda Takeshi; Imai Toshio; Inoue Asuka; Mimuro Hitomi; Maeda Yuichi; Kayama Hisako; Okumura Ryu; Aoki Junken; Okada Nobuhiko; Kida Toshiyuki; Ishii Masaru; Nabeshima Ryusuke; Takeda Kiyoshi;

  • 作者单位

    Osaka Univ, Grad Sch Med & Frontier Biosci, Dept Immunol & Cell Biol, Suita, Osaka, Japan;

    Tohoku Univ, Grad Sch Pharmaceut Sci, Sendai, Miyagi, Japan;

    Japan Agcy Med Res & Dev, Core Res Evolut Sci & Technol, Tokyo, Japan;

    Tokyo Univ Agr & Technol, Grad Sch Agr, Dept Appl Biol Sci, Fuchu, Tokyo, Japan;

    Kitasato Univ, Sch Pharm, Dept Microbiol, Tokyo, Japan;

    Osaka Univ, WPI Immunol Frontier Res Ctr, Suita, Osaka, Japan;

    Univ Tokyo, Inst Med Sci, Int Res Ctr Infect Dis, Div Bacteriol, Tokyo, Japan;

    Osaka Univ, Inst Open & Transdisciplinary Res Initiat, Integrated Frontier Res Med Sci Div, Suita, Osaka, Japan;

    Osaka Univ, Grad Sch Med, Dept Microbiol & Immunol, Suita, Osaka, Japan;

    Osaka Univ, Grad Sch Engn, Dept Appl Chem, Suita, Osaka, Japan;

    Osaka Univ, Res Inst Microbial Dis, Dept Infect Microbiol, Suita, Osaka, Japan;

    Ono Pharmaceut Co Ltd, Exploratory Res Labs, Osaka, Japan;

    KAN Res Inst, Kobe, Hyogo, Japan;

    Osaka Univ, Grad Sch Med, Dept Resp Med & Clin Immunol, Suita, Osaka, Japan;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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