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首页> 外文期刊>Diabetes >Promotion of Autoimmune Diabetes by Cereal Diet in the Presence or Absence of Microbes Associated With Gut Immune Activation, Regulatory Imbalance, and Altered Cathelicidin Antimicrobial Peptide
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Promotion of Autoimmune Diabetes by Cereal Diet in the Presence or Absence of Microbes Associated With Gut Immune Activation, Regulatory Imbalance, and Altered Cathelicidin Antimicrobial Peptide

机译：在存在或不存在与肠道免疫激活，调节失衡和改变的Cathelicidin抗菌肽相关的微生物的情况下，通过谷物饮食促进自身免疫性糖尿病

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摘要

We are exposed to millions of microbial and dietary antigens via the gastrointestinal tract, which likely play a key role in type 1 diabetes (T1D). We differentiated the effects of these two major environmental factors on gut immunity and T1D. Diabetes-prone BioBreeding (BBdp) rats were housed in specific pathogen-free (SPF) or germ-free (GF) conditions and weaned onto diabetes-promoting cereal diets or a protective low-antigen hydrolyzed casein (HC) diet, and T1D incidence was monitored. Fecal microbiota 16S rRNA genes, immune cell distribution, and gene expression in the jejunum were analyzed. T1D was highest in cereal-SPF (65%) and cereal-GF rats (53%) but inhibited and delayed in HC-fed counterparts. Nearly all HC-GF rats remained diabetes-free, whereas HC-fed SPF rats were less protected (7 vs. 29%). Bacterial communities differed in SPF rats fed cereal compared with HC. Cereal-SPF rats displayed increased gut CD3~+ and CD8α~+ lymphocytes, ratio of Ifng to π-4RNA, and Lck expression, indicating T-cell activation. The ratio of CD3~+ T cells expressing the T_(reg) marker Foxp3~+ was highest in HC-GF and lowest in cereal-SPF rats. Resident CD163~+ M2 macrophages were increased in HC-protected rats. The cathelicidin antimicrobial peptide (Camp) gene was upregulated in the jejunum of HC diet-protected rats, and CAMP~+ cells colocalized with CD163. A cereal diet was a stronger promoter of T1D than gut microbes in association with impaired gut immune homeostasis.
机译：我们通过胃肠道接触了数百万种微生物和饮食抗原，这些抗原可能在1型糖尿病（T1D）中起关键作用。我们区分了这两个主要环境因素对肠道免疫和T1D的影响。将易患糖尿病的生物繁殖（BBdp）大鼠置于特定的无病原体（SPF）或无菌（GF）的条件下，并断奶至促进糖尿病的谷物饮食或保护性的低抗原水解酪蛋白（HC）饮食中，并降低T1D发生率被监视。分析粪便微生物群16S rRNA基因，免疫细胞分布和空肠中的基因表达。 T1D在谷类-SPF大鼠（65％）和谷类-GF大鼠（53％）中最高，但在HC喂养的同伴中被抑制和延迟。几乎所有HC-GF大鼠均保持无糖尿病状态，而HC喂养的SPF大鼠受到的保护较小（7％vs. 29％）。与HC相比，饲喂谷物的SPF大鼠细菌群落不同。谷物-SPF大鼠的肠道CD3〜+和CD8α〜+淋巴细胞增多，Ifng与π-4RNA的比率以及Lck表达，表明T细胞活化。表达T_（reg）标记Foxp3〜+的CD3〜+ T细胞比例在HC-GF中最高，而在谷物SPF大鼠中最低。 HC保护的大鼠体内CD163〜+ M2巨噬细胞数量增加。在饮食保护的HC大鼠的空肠中，cathelicidin抗菌肽（Camp）基因被上调，并且CAMP〜+细胞与CD163共定位。谷物饮食比肠道微生物更能促进T1D的发生，与肠道免疫稳态受损有关。

著录项

  • 来源
    《Diabetes》 |2013年第6期|2036-2047|共12页
  • 作者

    Christopher Patrick; Gen-Sheng Wang; David E. Lefebvre; Jennifer A. Crookshank; Brigitte Sonier; Chandra Eberhard; Majid Mojibian; Christopher R. Kennedy; Stephen P.J. Brooks; Martin L. Kalmokoff; Mariantonia Maglio; Riccardo Troncone; Philippe Poussier; Fraser W. Scott;

  • 作者单位

    Chronic Disease Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada,Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, Ontario, Canada;

    Chronic Disease Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada;

    Chronic Disease Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada,Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, Ontario, Canada;

    Chronic Disease Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada;

    Chronic Disease Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada;

    Chronic Disease Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada,Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, Ontario, Canada;

    Chronic Disease Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada,Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, Ontario, Canada;

    Chronic Disease Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada,Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Ontario, Canada,European Laboratory for the Investigation of Food-Induced Diseases, University Federico II, Naples, Italy;

    Nutrition Research Division, Health Canada, Ottawa, Ontario, Canada;

    Atlantic Food and Horticulture Centre, Agriculture and Agri-Food Canada, Kentville, Nova Scotia, Canada;

    European Laboratory for the Investigation of Food-Induced Diseases, University Federico II, Naples, Italy;

    European Laboratory for the Investigation of Food-Induced Diseases, University Federico II, Naples, Italy;

    Sunnybrook Health Sciences Centre, Toronto, Ontario, Canada;

    Chronic Disease Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada,Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, Ontario, Canada,Department of Medicine, University of Ottawa, Ottawa, Ontario, Canada;

  • 收录信息 美国《科学引文索引》(SCI);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
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  • 入库时间 2022-08-18 03:46:25

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