背景:肠道菌群被认为是代谢疾病的主要调节因子。这调和了代谢炎症的概念和疾病的流行发展。除了证据表明特定的肠道微生物群是肥胖患者的特征之外,2型糖尿病,和肝脏脂肪变性,致病的机制可能与微生物从肠道到组织的易位有关,诱导炎症。调节这种过程的机制基于肠道微生物群和宿主免疫系统之间的串扰。进化的全基因组理论支持这一概念,并暗示旨在控制血糖的治疗策略应同时考虑肠道微生物群和宿主免疫系统。
方法:这篇综述讨论了关于肠道菌群对宿主免疫系统串扰的双向影响的最新证据,以控制代谢性疾病。高血糖症,和肥胖。为了避免文献冗余,我们将把注意力集中在肠道免疫系统上,确定新治疗策略产生的证据,这可能是基于对肠道细菌向组织易位的控制。这种新策略应该阻碍肠道微生物群菌群失调在代谢性炎症发展中的作用。
结论:最近在啮齿动物中的证据使我们得出结论,肠道免疫系统受损是代谢疾病发展的特征,并可能是其原因。对分子机制的深刻理解应该允许开发针对代谢性疾病及其合并症的一线治疗方法。本文是有关微生物群的特刊的一部分。
BACKGROUND: Gut microbiota is considered as a major regulator of metabolic disease. This reconciles the notion of metabolic inflammation and the epidemic development of the disease. In addition to evidence showing that a specific gut microbiota characterizes patients with obesity, type 2 diabetes, and hepatic steatosis, the mechanisms causal to the disease could be related to the translocation of microbiota from the gut to the tissues, inducing inflammation. The mechanisms regulating such a process are based on the crosstalk between the gut microbiota and the host immune system. The hologenome theory of evolution supports this concept and implies that therapeutic strategies aiming to control glycemia should take into account both the gut microbiota and the host immune system.
METHODS: This review discusses the latest evidence regarding the bidirectional impact of the gut microbiota on host immune system crosstalk for the control of metabolic disease, hyperglycemia, and obesity. To avoid redundancies with the literature, we will focus our attention on the intestinal immune system, identifying evidence for the generation of novel therapeutic strategies, which could be based on the control of the translocation of gut bacteria to tissues. Such novel strategies should hamper the role played by gut microbiota dysbiosis on the development of metabolic inflammation.
CONCLUSIONS: Recent evidence in rodents allows us to conclude that an impaired intestinal immune system characterizes and could be causal in the development of metabolic disease. The fine understanding of the molecular mechanisms should allow for the development of a first line of treatment for metabolic disease and its co-morbidities. This article is part of a special issue on microbiota.