Immuno-microbiota cross and talk: The new paradigm of metabolic diseases

被引:106
作者
Burcelin, Remy [1 ,2 ]
Garidou, Lucile [1 ,2 ]
Pomie, Celine [1 ,2 ]
机构
[1] INSERM, U1048, Inst Malad Metabol & Cardiovasc I2MC, F-31432 Toulouse, France
[2] Univ Toulouse 3, F-31432 Toulouse 4, France
关键词
Intestinal microbiota; Innate immunity; Metabolic diseases; Diabetes; Obesity; DIET-INDUCED OBESITY; REGULATORY T-CELLS; HIGH-FAT-DIET; LIPOPOLYSACCHARIDE-BINDING-PROTEIN; II DIABETES-MELLITUS; WHITE ADIPOSE-TISSUE; INSULIN-RESISTANCE; GUT MICROBIOTA; DENDRITIC CELLS; MACROPHAGE INFILTRATION;
D O I
10.1016/j.smim.2011.11.011
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Over the last decades the rising occurrence of metabolic diseases throughout the world points to the failure of preventive and therapeutic strategies and of the corresponding molecular and physiological concepts. Therefore, a new paradigm needs to be elucidated. Very recently the intimate cross talk of the intestinal microbiota with the host immune system has opened new avenues. The large diversity of the intestinal microbes' genome, i.e. the metagenome, and the extreme plasticity of the immune system provide a unique balance which, when finely tuned, maintains a steady homeostasis. The discovery that a new microbiota repertoire is one of the causes responsible for the onset of metabolic disease suggests that the relationship with the immune system is impaired. Therefore, we here review the recent arguments that support the view that an alteration in the microbiota to host immune system balance leads to an increased translocation of bacterial antigens towards metabolically active tissues, and could result in a chronic inflammatory state and consequently impaired metabolic functions such as insulin resistance, hepatic fat deposition, insulin unresponsiveness, and excessive adipose tissue development. This imbalance could be at the onset of metabolic disease, and therefore the early treatment of the microbiota dysbiosis or immunomodulatory strategies should prevent and slow down the epidemic of metabolic diseases and hence the corresponding lethal cardiovascular consequences. (C) 2011 Published by Elsevier Ltd.
引用
收藏
页码:67 / 74
页数:8
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