Etienne-Mesmin Lucie, Chassaing Benoit, Gewirtz Andrew T
Lucie Etienne-Mesmin, Benoit Chassaing, Andrew T Gewirtz, Center for Inflammation, Immunity, and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA 30303, United States.
World J Gastrointest Pharmacol Ther. 2017 Feb 6;8(1):7-9. doi: 10.4292/wjgpt.v8.i1.7.
Inflammatory bowel diseases (IBD), which comprise Crohn's disease and ulcerative colitis, are chronic intestinal disorders with an increased prevalence and incidence over the last decade in many different regions over the world. The etiology of IBD is still not well defined, but evidence suggest that it results from perturbation of the homeostasis between the intestinal microbiota and the mucosal immune system, with the involvement of both genetic and environmental factors. Genome wide association studies, which involve large-scale genome-wide screening of potential polymorphism, have identified several mutations associated with IBD. Among them, , a gene encoding an adapter molecule involved in innate immune response to fungi ( type C-lectin sensing) through the activation of IL-22 signaling pathway, has been identified as one IBD susceptible genes. Dietary compounds, which represent a source of energy and metabolites for gut bacteria, are also appreciated to be important actors in the etiology of IBD, for example by altering gut microbiota composition and by regulating the generation of short chain fatty acids. A noteworthy study published in the June 2016 issue of by Lamas and colleagues investigates the interaction between and the gut microbiota in the generation of the microbiota-derived tryptophan metabolite. This study highlights the role of tryptophan in dampening intestinal inflammation in susceptible hosts.
炎症性肠病(IBD)包括克罗恩病和溃疡性结肠炎,是一种慢性肠道疾病,在过去十年中,其在世界许多不同地区的患病率和发病率都有所上升。IBD的病因仍未完全明确,但有证据表明,它是由肠道微生物群与黏膜免疫系统之间的稳态失衡导致的,涉及遗传和环境因素。全基因组关联研究涉及对潜在多态性进行大规模全基因组筛查,已经确定了几个与IBD相关的突变。其中,一个编码衔接分子的基因,该衔接分子通过激活IL-22信号通路参与对真菌的固有免疫反应(C型凝集素感应),已被确定为一个IBD易感基因。膳食化合物是肠道细菌的能量和代谢物来源,也被认为是IBD病因中的重要因素,例如通过改变肠道微生物群组成和调节短链脂肪酸的生成。拉马斯及其同事在2016年6月出版的《 》上发表的一项值得注意的研究,调查了 在微生物群衍生的色氨酸代谢产物生成过程中与肠道微生物群之间的相互作用。这项研究突出了色氨酸在减轻易感宿主肠道炎症中的作用。