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饮食中硫脂衍生的磺基喹诺糖对易患结肠炎的白细胞介素-10缺陷小鼠肠道微生物群组成和炎症状态的影响。

Impact of dietary sulfolipid-derived sulfoquinovose on gut microbiota composition and inflammatory status of colitis-prone interleukin-10-deficient mice.

作者信息

Burkhardt Wiebke, Rausch Theresa, Klopfleisch Robert, Blaut Michael, Braune Annett

机构信息

Research Group Intestinal Microbiology, Department of Molecular Toxicology, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal, Germany.

Institute of Veterinary Pathology, Freie Universitaet Berlin, Berlin, Germany.

出版信息

Int J Med Microbiol. 2021 Apr;311(3):151494. doi: 10.1016/j.ijmm.2021.151494. Epub 2021 Feb 25.

DOI:10.1016/j.ijmm.2021.151494
PMID:33711649
Abstract

The interplay between diet, intestinal microbiota and host is a major factor impacting health. A diet rich in unsaturated fatty acids has been reported to stimulate the growth of Bilophila wadsworthia by increasing the proportion of the sulfonated bile acid taurocholate (TC). The taurine-induced overgrowth of B. wadsworthia promoted the development of colitis in interleukin-10-deficient (IL-10) mice. This study aimed to investigate whether intake of the sulfonates sulfoquinovosyl diacylglycerols (SQDG) with a dietary supplement or their degradation product sulfoquinovose (SQ), stimulate the growth of B. wadsworthia in a similar manner and, thereby, cause intestinal inflammation. Conventional IL-10 mice were fed a diet supplemented with the SQDG-rich cyanobacterium Arthrospira platensis (Spirulina). SQ or TC were orally applied to conventional IL-10 mice and gnotobiotic IL-10 mice harboring a simplified human intestinal microbiota with or without B. wadsworthia. Analyses of inflammatory parameters revealed that none of the sulfonates induced severe colitis, but both, Spirulina and TC, induced expression of pro-inflammatory cytokines in cecal mucosa. Cell numbers of B. wadsworthia decreased almost two orders of magnitude by Spirulina feeding but slightly increased in gnotobiotic SQ and conventional TC mice. Changes in microbiota composition were observed in feces as a result of Spirulina or TC feeding in conventional mice. In conclusion, the dietary sulfonates SQDG and their metabolite SQ did not elicit bacteria-induced intestinal inflammation in IL-10 mice and, thus, do not promote colitis.

摘要

饮食、肠道微生物群与宿主之间的相互作用是影响健康的主要因素。据报道,富含不饱和脂肪酸的饮食会通过增加磺化胆汁酸牛磺胆酸盐(TC)的比例来刺激沃兹沃思嗜胆菌的生长。牛磺酸诱导的沃兹沃思嗜胆菌过度生长促进了白细胞介素-10缺陷(IL-10)小鼠结肠炎的发展。本研究旨在调查摄入含有磺基喹喔啉二酰基甘油(SQDG)的膳食补充剂或其降解产物磺基喹喔啉糖(SQ)是否会以类似方式刺激沃兹沃思嗜胆菌的生长,从而导致肠道炎症。给常规IL-10小鼠喂食添加了富含SQDG的蓝藻钝顶螺旋藻(螺旋藻)的饮食。将SQ或TC口服应用于常规IL-10小鼠以及定殖有简化人类肠道微生物群且有或无沃兹沃思嗜胆菌的无菌IL-10小鼠。炎症参数分析表明,这些磺酸盐均未诱发严重结肠炎,但螺旋藻和TC均诱导了盲肠黏膜中促炎细胞因子的表达。通过喂食螺旋藻,沃兹沃思嗜胆菌的细胞数量减少了近两个数量级,但在无菌SQ小鼠和常规TC小鼠中略有增加。在常规小鼠中,由于喂食螺旋藻或TC,粪便中的微生物群组成发生了变化。总之,膳食磺酸盐SQDG及其代谢产物SQ在IL-10小鼠中未引发细菌诱导的肠道炎症,因此不会促进结肠炎。

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引用本文的文献

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Sulfoquinovose is exclusively metabolized by the gut microbiota and degraded differently in mice and humans.磺基喹诺糖仅由肠道微生物群代谢,在小鼠和人类中的降解方式不同。
Microbiome. 2025 Aug 7;13(1):184. doi: 10.1186/s40168-025-02175-x.
2
Bacterial microcompartments and energy metabolism drive gut colonization by Bilophila wadsworthia.细菌微区室与能量代谢促进沃兹沃思嗜胆菌在肠道的定殖。
Nat Commun. 2025 May 30;16(1):5049. doi: 10.1038/s41467-025-60180-y.
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New insights into the interplay between intestinal flora and bile acids in inflammatory bowel disease.
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An Alternative Approach for the Synthesis of Sulfoquinovosyldiacylglycerol.磺基奎诺糖二酰基甘油的一种替代合成方法。
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Systems Biology and Bile Acid Signalling in Microbiome-Host Interactions in the Cystic Fibrosis Lung.系统生物学与囊性纤维化肺部微生物群-宿主相互作用中的胆汁酸信号传导
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