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Gastroenterology:健康肠道菌群有助预防代谢综合征

来源:生物谷 2014-11-26 13:55

2014年11月26日讯 /生物谷BIOON/ --根据佐治亚州立大学和康奈尔大学研究人员证实:居住在肠道内的有助健康的肠道菌群,可以帮助治疗或预防代谢综合征。他们的研究结果发表在Gastroenterology杂志上。

他们证实,肠上皮细胞缺乏Toll样受体5,肠道菌群组合发生改变,而这会促进低度炎症和代谢综合征,变化后的细菌种群更具侵略性,会产生鞭毛蛋白和脂多糖等物质,进一步促进炎症。

在美国,代谢综合征影响34%的成年人。当一个人有这样的危险因素时:一个大腰围,高甘油三酯水平,低HDL胆固醇水平,高血压和高空腹血糖,会被诊断为患有代谢综合征。

一旦患上代谢综合征,发生心脏疾病和糖尿病的风险也增加。由于代谢综合征正变得越来越普遍,科学家们正在探索其中可能的原因。在先前发表在Science杂志上的研究中,Gewirtz和其他研究人员发现肠道菌群的改变对引发代谢综合征有促进作用。

肠道菌群在健康中发挥关键功能,当它变得失调,它会促进慢性炎症性疾病,如克罗恩病和溃疡性结肠炎。此外,肠道菌群改变会促进炎症,导致代谢综合征。(生物谷Bioon.com)

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Intestinal Epithelial Cell Toll-like Receptor 5 Regulates the Intestinal Microbiota to Prevent Low-Grade Inflammation and Metabolic Syndrome in Mice

Benoit Chassaing, Ruth E. Ley, Andrew T. Gewirtzemail

Background & Aims
Mice lacking the receptor Toll-like receptor 5 (TLR5-null mice), which recognizes flagellin, have an altered intestinal microbiota composition compared with wild-type mice; they develop low-grade inflammation and metabolic syndrome and are prone to colitis. The relative roles of intestinal epithelial cell (IEC) vs dendritic cell (DC) TLR5 in mediating these phenotypes are not clear; modification of intestinal microbiota composition has been reported to reflect animal husbandry practices rather than loss of TLR5. We generated mice with specific disruption of Tlr5 in IECs or DCs by using a breeding scheme that allows comparison with cohoused siblings as controls.

Methods
We generated C57BL/6 mice with LoxP sites flanking Tlr5. These mice were crossed with mice expressing Cre recombinase, regulated by the villin or CD11c promoters, to generate mice that lacked expression of TLR5 by IECs (TLR5ΔIEC) or DCs (TLR5ΔDC), respectively. Tlr5fl/fl siblings were used as controls. On weaning, mice were housed by sex and genotype or by sex only (genotypes cohoused). Mice were examined for basal phenotypes, including microbiota composition; we also analyzed responses to pathobiont challenge, administration of dextran sodium sulfate, and high-fat diets.

Results
Similar to previous findings from TLR5-null mice, TLR5ΔIEC mice had low-grade inflammation (mild splenomegaly, shortened colons, and increased fecal levels of lipocalin 2), metabolic syndrome, and an inability to clear pathobionts and were prone to developing colitis compared with their sibling controls under both housing conditions. Development of this inflammation in the TLR5ΔIEC mice was eliminated by administration of antibiotics and associated with alterations in localization of microbiota and levels of fecal lipopolysaccharide and flagellin. The composition of the microbiota clustered more closely according to genotype than housing. Loss of TLR5 from DCs did not associate with development of inflammation-associated phenotypes or alterations in the composition of the microbiota but resulted in complete loss of flagellin-induced production of interleukin-22.

Conclusions
In mice, flagellin activation of TLR5 on DCs leads to production of interleukin-22. Expression of TLR5 on IECs regulates the composition and localization of the intestinal microbiota, preventing diseases associated with intestinal inflammation.

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