首页> 美国卫生研究院文献>Nutrients >Undigested Food and Gut Microbiota May Cooperate in the Pathogenesis of Neuroinflammatory Diseases: A Matter of Barriers and a Proposal on the Origin of Organ Specificity
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Undigested Food and Gut Microbiota May Cooperate in the Pathogenesis of Neuroinflammatory Diseases: A Matter of Barriers and a Proposal on the Origin of Organ Specificity

机译:未消化的食物和肠道菌群可能在神经炎性疾病的发病机制中合作:障碍的一个问题和器官特异性起源的建议。

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摘要

As food is an active subject and may have anti-inflammatory or pro-inflammatory effects, dietary habits may modulate the low-grade neuroinflammation associated with chronic neurodegenerative diseases. Food is living matter different from us, but made of our own nature. Therefore, it is at the same time foreign to us ( ), if not yet digested, and like us ( ), after its complete digestion. To avoid the efflux of undigested food from the lumen, the intestinal barrier must remain intact. What and how much we eat shape the composition of gut microbiota. Gut dysbiosis, as a consequence of Western diets, leads to intestinal inflammation and a leaky intestinal barrier. The efflux of undigested food, microbes, endotoxins, as well as immune-competent cells and molecules, causes chronic systemic inflammation. Opening of the blood-brain barrier may trigger microglia and astrocytes and set up neuroinflammation. We suggest that what determines the organ specificity of the autoimmune-inflammatory process may depend on food antigens resembling proteins of the organ being attacked. This applies to the brain and neuroinflammatory diseases, as to other organs and other diseases, including cancer. Understanding the cooperation between microbiota and undigested food in inflammatory diseases may clarify organ specificity, allow the setting up of adequate experimental models of disease and develop targeted dietary interventions.
机译:由于食物是活跃的对象,并且可能具有抗炎或促炎作用,所以饮食习惯可能会调节与慢性神经退行性疾病相关的低度神经炎症。食物是与我们不同的生命,而是由我们自己的天性构成的。因此,在完全消化之后,如果尚未消化的话,它对我们()同时是陌生的,并且与我们()一样。为了避免未消化食物从管腔流出,肠屏障必须保持完整。我们吃什么和多少决定了肠道菌群的组成。西方饮食导致肠道内营养不良,导致肠道炎症和肠屏障渗漏。未消化的食物,微生物,内毒素以及具有免疫功能的细胞和分子的流出会导致慢性全身性炎症。血脑屏障的打开可能会触发小胶质细胞和星形胶质细胞并引起神经炎症。我们建议确定自身免疫炎症过程的器官特异性的因素可能取决于类似于被攻击器官蛋白质的食物抗原。这适用于脑部和神经炎性疾病,以及其他器官和其他疾病,包括癌症。了解微生物群和未消化食物在炎症性疾病中的合作可能会阐明器官特异性,允许建立适当的疾病实验模型并制定有针对性的饮食干预措施。

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