Basson Abigail, Trotter Ashley, Rodriguez-Palacios Alex, Cominelli Fabio
Digestive Health Research Institute, Case Western Reserve University , Cleveland, OH , USA.
Digestive Health Research Institute, Case Western Reserve University, Cleveland, OH, USA; University Hospitals Case Medical Center, Cleveland, OH, USA.
Front Immunol. 2016 Aug 2;7:290. doi: 10.3389/fimmu.2016.00290. eCollection 2016.
Numerous reviews have discussed gut microbiota composition changes during inflammatory bowel diseases (IBD), particularly Crohn's disease (CD). However, most studies address the observed effects by focusing on studying the univariate connection between disease and dietary-induced alterations to gut microbiota composition. The possibility that these effects may reflect a number of other interconnected (i.e., pantropic) mechanisms, activated in parallel, particularly concerning various bacterial metabolites, is in the process of being elucidated. Progress seems, however, hampered by various difficult-to-study factors interacting at the mucosal level. Here, we highlight some of such factors that merit consideration, namely: (1) the contribution of host genetics and diet in altering gut microbiome, and in turn, the crosstalk among secondary metabolic pathways; (2) the interdependence between the amount of dietary fat, the fatty acid composition, the effects of timing and route of administration on gut microbiota community, and the impact of microbiota-derived fatty acids; (3) the effect of diet on bile acid composition, and the modulator role of bile acids on the gut microbiota; (4) the impact of endogenous and exogenous intestinal micronutrients and metabolites; and (5) the need to consider food associated toxins and chemicals, which can introduce confounding immune modulating elements (e.g., antioxidant and phytochemicals in oils and proteins). These concepts, which are not mutually exclusive, are herein illustrated paying special emphasis on physiologically inter-related processes.
众多综述讨论了炎症性肠病(IBD),尤其是克罗恩病(CD)期间肠道微生物群组成的变化。然而,大多数研究通过关注疾病与饮食诱导的肠道微生物群组成变化之间的单变量联系来探讨观察到的影响。这些影响可能反映了许多其他相互关联(即泛向性)的机制同时被激活,特别是关于各种细菌代谢产物,这一可能性正在被阐明。然而,进展似乎受到在黏膜水平相互作用的各种难以研究的因素的阻碍。在此,我们强调一些值得考虑的此类因素,即:(1)宿主遗传学和饮食在改变肠道微生物组方面的作用,以及反过来,次级代谢途径之间的相互作用;(2)膳食脂肪量、脂肪酸组成、给药时间和途径对肠道微生物群群落的影响以及微生物衍生脂肪酸的影响之间的相互依存关系;(3)饮食对胆汁酸组成的影响,以及胆汁酸对肠道微生物群的调节作用;(4)内源性和外源性肠道微量营养素和代谢产物的影响;以及(5)需要考虑与食物相关的毒素和化学物质,它们可能引入混杂的免疫调节元素(例如,油和蛋白质中的抗氧化剂和植物化学物质)。这些并非相互排斥的概念在此处进行阐述,并特别强调生理上相互关联的过程。