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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Regulation of induced colonic inflammation by Lactobacillus acidophilus deficient in lipoteichoic acid
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Regulation of induced colonic inflammation by Lactobacillus acidophilus deficient in lipoteichoic acid

机译：缺乏脂蛋白酸的嗜酸乳杆菌对诱导性结肠炎症的调节

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摘要

Imbalance in the regulatory immune mechanisms that control intestinal cellular and bacterial homeostasis may lead to induction of the detrimental inflammatory signals characterized in humans as inflammatory bowel disease. Induction of proinflammatory cytokines (i.e., IL-12) induced by dendritic cells (DCs) expressing pattern recognition receptors may skew naive T cells to T helper 1 polarization, which is strongly implicated in mucosal autoimmu-nity. Recent studies show the ability of probiotic microbes to treat and prevent numerous intestinal disorders, including Clostridium difficile-induced colitis. To study the molecular mechanisms involved in the induction and repression of intestinal inflammation, the phosphoglycerol transferase gene that plays a key role in lipoteichoic acid (LTA) biosynthesis in Lactobacillus acidophilus NCFM (NCK56) was deleted. The data show that the L acidophilus LTA-negative in LTA (NCK2025) not only down-regulated IL-12 and TNFa but also significantly enhanced IL-10 in DCs and controlled the regulation of costimulatory DC functions, resulting in their inability to induce CD4+ T-cell activation. Moreover, treatment of mice with NCK2025 compared with NCK56 significantly mitigated dextran sulfate sodium and CD4+CD45RBhighT cell-induced colitis and effectively ameliorated dextran sulfate sodium-established colitis through a mechanism that involves IL-10 and CD4+FoxP3+ T regulatory cells to dampen exaggerated mucosal inflammation. Directed alteration of cell surface components of L. acidophilus NCFM establishes a potential strategy for the treatment of inflammatory intestinal disorders.
机译：控制肠道细胞和细菌稳态的调节性免疫机制的失衡可能导致诱导有害的炎症信号，人体以炎症性肠病为特征。表达模式识别受体的树突状细胞（DC）诱导的促炎性细胞因子（即IL-12）的诱导可能会使未成熟的T细胞偏向T辅助1极化，这与粘膜自身免疫性密切相关。最近的研究表明益生菌具有治疗和预防多种肠道疾病的能力，包括艰难梭菌诱导的结肠炎。为了研究诱导和抑制肠道炎症的分子机制，删除了在嗜酸乳杆菌NCFM（NCK56）的脂磷壁酸（LTA）生物合成中起关键作用的磷酸甘油转移酶基因。数据显示LTA中的嗜酸乳杆菌LTA阴性（NCK2025）不仅下调了IL-12和TNFa，而且还显着增强了DC中的IL-10并控制了共刺激DC功能的调节，导致它们无法诱导CD4 + T细胞活化。此外，与NCK56相比，用NCK2025进行的小鼠治疗显着减轻了葡聚糖硫酸钠和CD4 + CD45RBhighT细胞诱导的结肠炎，并通过涉及IL-10和CD4 + FoxP3 + T调节细胞的机制减轻了葡聚糖硫酸钠建立的结肠炎，从而减轻了夸张的作用。粘膜炎症。嗜酸乳杆菌NCFM的细胞表面成分的直接改变建立了治疗炎症性肠道疾病的潜在策略。

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    Mansour Mohamadzadeh; Erika A. Pfeiler; Jeffrey B. Brown; Mojgan Zadeh; Matthew Gramarossa; Elizabeth Managlia; Praveen Bere; Bara Sarraj; Mohammad W. Khan; Krishna Chaitanya Pakanati; M. Javeed Ansari; Sarah OFlaherty; Terrence Barrett; Todd R. Klaenhammer;

  • 作者单位

    Northwestern University, The Feinberg School of Medicine, Chicago, IL 60611;

    Genomic Sciences Graduate Program, North Carolina State University,Raleigh, NC,Department of Food, Bioprocessing and Nutrition Sciences, North Carolina State University, Raleigh, NC 27695;

    Northwestern University, The Feinberg School of Medicine, Chicago, IL 60611;

    Northwestern University, The Feinberg School of Medicine, Chicago, IL 60611;

    Northwestern University, The Feinberg School of Medicine, Chicago, IL 60611;

    Northwestern University, The Feinberg School of Medicine, Chicago, IL 60611;

    Northwestern University, The Feinberg School of Medicine, Chicago, IL 60611;

    Northwestern University, The Feinberg School of Medicine, Chicago, IL 60611;

    Northwestern University, The Feinberg School of Medicine, Chicago, IL 60611;

    Northwestern University, The Feinberg School of Medicine, Chicago, IL 60611;

    Northwestern University, The Feinberg School of Medicine, Chicago, IL 60611;

    Department of Food, Bioprocessing and Nutrition Sciences, North Carolina State University, Raleigh, NC 27695;

    Northwestern University, The Feinberg School of Medicine, Chicago, IL 60611;

    Genomic Sciences Graduate Program, North Carolina State University,Raleigh, NC,Department of Food, Bioprocessing and Nutrition Sciences, North Carolina State University, Raleigh, NC 27695;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    antiinflammatory; lactobacilli; toll-like receptor 2; innate immunity;

    机译：抗炎;乳杆菌;Toll样受体2;先天免疫;

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