Role of Metabolic Endotoxemia in Systemic Inflammation and Potential Interventions

被引:342
作者
Mohammad, Shireen [1 ]
Thiemermann, Christoph [1 ]
机构
[1] Queen Mary Univ London, William Harvey Res Inst, London, England
关键词
metabolic endotoxemia; lipopolysaccharide; high-fat diet; Toll-like receptor; antimicrobial peptides; gut permeability; HIGH-FAT DIET; ANTIMICROBIAL PEPTIDES; GUT MICROBIOTA; TIGHT JUNCTIONS; PERMEABILITY; RECEPTOR; OBESITY; ACTIVATION; MECHANISMS; RESISTANCE;
D O I
10.3389/fimmu.2020.594150
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Diet-induced metabolic endotoxemia is an important factor in the development of many chronic diseases in animals and man. The gut epithelium is an efficient barrier that prevents the absorption of liposaccharide (LPS). Structural changes to the intestinal epithelium in response to dietary alterations allow LPS to enter the bloodstream, resulting in an increase in the plasma levels of LPS (termed metabolic endotoxemia). LPS activates Toll-like receptor-4 (TLR4) leading to the production of numerous pro-inflammatory cytokines and, hence, low-grade systemic inflammation. Thus, metabolic endotoxemia can lead to several chronic inflammatory conditions. Obesity, diabetes, and non-alcoholic fatty liver disease (NAFLD) can also cause an increase in gut permeability and potential pharmacological and dietary interventions could be used to reduce the chronic low-grade inflammation associated with endotoxemia.
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页数:16
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