PDF(Pubmed)
Abstract：
Ulcerative colitis (UC) is an autoimmune disease in which the immune system attacks the colon, leading to ulcer development, loss of colon function, and bloody diarrhea. The human gut ecosystem consists of almost 2000 different species of bacteria, forming a bioreactor fueled by dietary micronutrients to produce bioreactive compounds, which are absorbed by our body and signal to distant organs. Studies have shown that the Western diet, with fewer short-chain fatty acids (SCFAs), can alter the gut microbiome composition and cause the host\'s epigenetic reprogramming. Additionally, overproduction of H2S from the gut microbiome due to changes in diet patterns can further activate pro-inflammatory signaling pathways in UC. This review discusses how the Western diet affects the microbiome\'s function and alters the host\'s physiological homeostasis and susceptibility to UC. This article also covers the epidemiology, prognosis, pathophysiology, and current treatment strategies for UC, and how they are linked to colorectal cancer.
摘要：
溃疡性结肠炎（UC）是一种自身免疫性疾病，其中免疫系统攻击结肠，导致溃疡发展，结肠功能丧失,和血性腹泻。人类肠道生态系统由近2000种不同的细菌组成，形成以膳食微量营养素为燃料的生物反应器，以产生生物活性化合物，它们被我们的身体吸收并向远处的器官发出信号。研究表明，西方饮食，短链脂肪酸（SCFA）较少，可以改变肠道微生物组组成并引起宿主的表观遗传重编程。此外,由于饮食模式的改变，肠道微生物组的H2S过量产生可以进一步激活UC的促炎信号通路。这篇综述讨论了西方饮食如何影响微生物组的功能并改变宿主的生理稳态和对UC的易感性。这篇文章还涵盖了流行病学，预后,病理生理学,以及目前UC的治疗策略，以及它们与结直肠癌的联系。
