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Selenium and inflammatory bowel disease

机译:硒和炎症性肠病

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Kudva AK, Shay AE, Prabhu KS. Selenium and inflammatory bowel disease. Dietary intake of the micronutrient selenium is essential for normal immune functions. Selenium is cotranslationally incorporated as the 21st amino acid, selenocysteine, into selenoproteins that function to modulate pathways involved in inflammation. Epidemiological studies have suggested an inverse association between selenium levels and inflammatory bowel disease (IBD), which includes Crohn's disease and ulcerative colitis that can potentially progress to colon cancer. However, the underlying mechanisms are not well understood. Here we summarize the current literature on the pathophysiology of IBD, which is multifactorial in origin with unknown etiology. We have focused on a few selenoproteins that mediate gastrointestinal inflammation and activate the host immune response, wherein macrophages play a pivotal role. Changes in cellular oxidative state coupled with altered expression of selenoproteins in macrophages drive the switch from a proinflammatory phenotype to an anti-inflammatory phenotype to efficiently resolve inflammation in the gut and restore epithelial barrier integrity. Such a phenotypic plasticity is accompanied by changes in cytokines, chemokines, and bioactive metabolites, including eicosanoids that not only mitigate inflammation but also partake in restoring gut homeostasis through diverse pathways involving differential regulation of transcription factors such as nuclear factor-kB and peroxisome proliferator-activated receptor-7. The role of the intestinal microbiome in modulating inflammation and aiding in selenium-dependent resolution of gut injury is highlighted to provide novel insights into the beneficial effects of selenium in IBD.
机译:Kudva AK,Shay Ae,Prabhu Ks。硒和炎症性肠病。微量营养素硒的膳食摄入对于正常的免疫功能至关重要。硒是CoT或称为21st氨基酸的硒细胞,进入硒蛋白,其能够调节炎症的途径。流行病学研究表明硒水平和炎症性肠病(IBD)之间的反比异性关联,包括克罗恩病和溃疡性结肠炎,可以潜在地进入结肠癌。然而,潜在机制并不熟知。在这里,我们总结了关于IBD的病理生理学的当前文献,这是源于未知病因的多因素。我们专注于一些硒蛋白,介导胃肠炎症并激活宿主免疫应答,其中巨噬细胞发挥枢轴作用。与巨噬细胞中硒蛋白的改变表达偶联的细胞氧化状态的变化驱动从促炎表型转化为抗炎表型以有效地解析肠道中的炎症并恢复上皮阻挡完整性。这种表型可塑性伴随着细胞因子,趋化因子和生物活性代谢物的变化,包括逐渐减轻炎症,而且还通过涉及核因子-Kb和过氧化物酶体增殖物等差异调节的不同途径来减轻炎症而且参与静态稳态。活化受体-7。突出显示肠道微生物组在调节炎症和依赖甲硒损伤的依赖性分辨率中的作用,以提供对IBD中硒的有益作用的新见解。

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