Burkhardt Wiebke, Rausch Theresa, Klopfleisch Robert, Blaut Michael, Braune Annett
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.
Int J Med Microbiol. 2021 Apr;311(3):151494. doi: 10.1016/j.ijmm.2021.151494. Epub 2021 Feb 25.
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.
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。