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High Fat Diet Causes Depletion of Intestinal Eosinophils Associated with Intestinal Permeability

机译：高脂饮食会导致与肠通透性相关的肠嗜酸性粒细胞减少

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The development of intestinal permeability and the penetration of microbial products are key factors associated with the onset of metabolic disease. However, the mechanisms underlying this remain unclear. Here we show that, unlike liver or adipose tissue, high fat diet (HFD)/obesity in mice does not cause monocyte/macrophage infiltration into the intestine or pro-inflammatory changes in gene expression. Rather HFD causes depletion of intestinal eosinophils associated with the onset of intestinal permeability. Intestinal eosinophil numbers were restored by returning HFD fed mice to normal chow and were unchanged in leptin-deficient (Ob/Ob) mice, indicating that eosinophil depletion is caused specifically by a high fat diet and not obesity per se. Analysis of different aspects of intestinal permeability in HFD fed and Ob/Ob mice shows an association between eosinophil depletion and ileal paracelullar permeability, as well as leakage of albumin into the feces, but not overall permeability to FITC dextran. These findings provide the first evidence that a high fat diet causes intestinal eosinophil depletion, rather than inflammation, which may contribute to defective barrier integrity and the onset of metabolic disease.
机译：肠道通透性的发展和微生物产品的渗透是与代谢疾病发作有关的关键因素。但是，其背后的机制仍不清楚。在这里，我们表明，与肝脏或脂肪组织不同，小鼠的高脂饮食（HFD）/肥胖症不会引起单核细胞/巨噬细胞向肠道的浸润或基因表达的促炎性变化。相反，HFD会导致肠道嗜酸性粒细胞耗竭，并伴有肠道通透性的开始。通过喂食HFD的小鼠恢复正常食物，可恢复肠道嗜酸性粒细胞的数量，而在缺乏瘦素的小鼠（Ob / Ob）中，肠道嗜酸性粒细胞的数量没有变化，这表明嗜酸性粒细胞的消耗是由高脂饮食而不是肥胖本身引起的。对HFD喂养和Ob / Ob小鼠的肠道通透性不同方面的分析显示，嗜酸性粒细胞消耗与回肠回肠旁囊通透性以及白蛋白渗入粪便之间存在关联，但对FITC葡聚糖的总体通透性​​却不相关。这些发现提供了第一个证据，即高脂肪饮食会导致肠道嗜酸性粒细胞耗竭而不是炎症，这可能会导致屏障完整性不良和代谢疾病的发作。

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