ALJahdali Nesreen, Gadonna-Widehem Pascale, Delayre-Orthez Carine, Marier David, Garnier Benjamin, Carbonero Franck, Anton Pauline M
Cell and Molecular Biology Program, University of Arkansas, 2650 Young Avenue, Fayetteville, AR, 72704, USA.
Expression des Gènes et Régulation Epigénétique par l'Aliment UP 2012.10.101., Institut Polytechnique UniLaSalle, 19 rue Pierre Waguet, 60000, Beauvais, France.
Dig Dis Sci. 2017 Dec;62(12):3370-3384. doi: 10.1007/s10620-017-4767-8. Epub 2017 Sep 30.
Diet is suggested to participate in the etiology of inflammatory bowel diseases (IBD). Repeated exposure to Maillard reaction products (MRPs), molecules resulting from reduction reactions between amino acids and sugars during food heating, has been reported to be either potentially detrimental or beneficial to health.
The aim of this study is to determine the effect of repeated oral ingestion of N -carboxymethyllysine (CML), an advanced MRP, on the onset of two models of experimental IBD and on the gut microbiota composition of mice.
Mice received either saline (control) or N -carboxymethyllysine daily for 21 days. For the last week of treatment, each group was split into subgroups, receiving dextran sulfate sodium salt (DSS) or trinitrobenzenesulfonic acid (TNBS) to induce colitis. Intensity of inflammation was quantified, and cecal microbiota characterized by bacterial 16S ribosomal RNA (rRNA) amplicon sequencing.
Daily oral administration of N -carboxymethyllysine did not induce intestinal inflammation and had limited impact on gut microbiota composition (Bacteroidaceae increase, Lachnospiraceae decrease). DSS and TNBS administration resulted in expected moderate experimental colitis with a shift of Bacteroidetes/Firmicutes ratio and a significant Proteobacteria increase but with distinct profiles: different Proteobacteria taxa for DSS, but mainly Enterobacteriaceae for TNBS. While N -carboxymethyllysine exposure failed to prevent the inflammatory response, it allowed maintenance of healthy gut microbiota profiles in mice treated with DSS (but not TNBS).
Repeated oral exposure to CML limits dysbiosis in experimental colitis. IBD patients may modulate their microbiota profile by regulating the level and type of dietary MRP consumption.
饮食被认为与炎症性肠病（IBD）的病因有关。据报道，反复接触美拉德反应产物（MRP），即食物加热过程中氨基酸和糖之间还原反应产生的分子，可能对健康有害或有益。
本研究旨在确定反复口服晚期MRP——N-羧甲基赖氨酸（CML）对两种实验性IBD模型发病及小鼠肠道微生物群组成的影响。
小鼠连续21天每天接受生理盐水（对照）或N-羧甲基赖氨酸。在治疗的最后一周，每组再分为亚组，接受葡聚糖硫酸钠（DSS）或三硝基苯磺酸（TNBS）诱导结肠炎。对炎症强度进行量化，并通过细菌16S核糖体RNA（rRNA）扩增子测序对盲肠微生物群进行表征。
每日口服N-羧甲基赖氨酸未诱发肠道炎症，对肠道微生物群组成的影响有限（拟杆菌科增加，毛螺菌科减少）。给予DSS和TNBS导致预期的中度实验性结肠炎，拟杆菌门/厚壁菌门比例发生变化，变形菌门显著增加，但具有不同的特征：DSS导致不同的变形菌门分类群增加，而TNBS主要导致肠杆菌科增加。虽然接触N-羧甲基赖氨酸未能预防炎症反应，但它能使接受DSS治疗的小鼠（而非TNBS治疗的小鼠）维持健康的肠道微生物群特征。
反复口服CML可限制实验性结肠炎中的菌群失调。IBD患者可通过调节饮食中MRP的摄入水平和类型来调节其微生物群特征。
