Long-term consumption of caffeine-free high sucrose cola beverages aggravates the pathogenesis of EAE in mice.

Long-term consumption of caffeine-free high sucrose cola beverages aggravates the pathogenesis of EAE in mice.
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长期饮用不含咖啡因的高蔗糖可乐饮料会加重小鼠EAE的发病。

DOI:
10.1038/celldisc.2017.20
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发表时间:
2017
期刊:
影响因子:
33.5
通讯作者:
Yin Z
Yin Z
中科院分区:
生物学1区
文献类型:
--
作者:
Cao G;Wang Q;Huang W;Tong J;Ye D;He Y;Liu Z;Tang X;Cheng H;Wen Q;Li D;Chau HT;Wen Y;Zhong H;Meng Z;Liu H;Wu Z;Zhao L;Flavell RA;Zhou H;Xu A;Yang H;Yin Z

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流行病学数据提供了强有力的证据表明,在过去的几十年中,许多自身免疫性疾病的发病率急剧增加,主要是在西方和西方化国家。最近的研究清楚地表明,“西方饮食”至少部分地通过破坏肠道紧密连接和改变微生物群的结构和代谢物来增加自身免疫性疾病的风险。然而,作为西方饮食中添加糖的主要来源之一的高蔗糖可乐饮料(HSCB)的作用却鲜为人知。最近,一项人群研究表明,经常饮用含糖饮料与女性血清阳性类风湿性关节炎的风险增加有关,这引起了人们对这些饮料对自身免疫性疾病发病机制及其潜在机制的真正影响的兴趣。在这里,我们表明,长期消费的无咖啡因的HSCBs加重了实验性自身免疫性脑脊髓炎的发病机制,在小鼠中的微生物菌群依赖的方式。进一步的研究表明,HSCBs改变了微生物群的群落结构,增加了Th17细胞。高蔗糖消耗具有类似的有害影响,而咖啡因污染限制了浸润的病原性免疫细胞并抵消了这些影响。这些结果揭示了脱咖啡因的HSCB在加重小鼠实验性自身免疫性脑脊髓炎的发病机制中的有害作用。
Epidemiological data provide strong evidence of dramatically increasing incidences of many autoimmune diseases in the past few decades, mainly in western and westernized countries. Recent studies clearly revealed that ‘Western diet’ increases the risk of autoimmune diseases at least partially via disrupting intestinal tight junctions and altering the construction and metabolites of microbiota. However, the role of high sucrose cola beverages (HSCBs), which are one of the main sources of added sugar in the western diet, is barely known. Recently, a population study showed that regular consumption of sugar-sweetened beverages is associated with increased risk of seropositive rheumatoid arthritis in women, which provokes interest in the genuine effects of these beverages on the pathogenesis of autoimmune diseases and the underlying mechanisms. Here we showed that long-term consumption of caffeine-free HSCBs aggravated the pathogenesis of experimental autoimmune encephalomyelitis in mice in a microbiota-dependent manner. Further investigation revealed that HSCBs altered community structure of microbiota and increased Th17 cells. High sucrose consumption had similar detrimental effects while caffeine contamination limited the infiltrated pathogenic immune cells and counteracted these effects. These results uncovered a deleterious role of decaffeinated HSCBs in aggravating the pathogenesis of experimental autoimmune encephalomyelitis in mice.