de Souza Heitor S P
aServiço de Gastroenterologia e Laboratório Multidisciplinar de Pesquisa, Departamento de Clínica Médica, Hospital Universitário Clementino Fraga Filho, Universidade Federal do Rio de Janeiro bD'Or Institute for Research and Education (IDOR), Rio de Janeiro, Rio de Janeiro, Brazil.
Curr Opin Gastroenterol. 2017 Jul;33(4):222-229. doi: 10.1097/MOG.0000000000000364.
Crohn's disease and ulcerative colitis, the two major forms of inflammatory bowel disease (IBD), represent chronic diseases of unknown cause, and they are regarded as prototypical complex diseases. Despite all the recent advances, a complete appreciation of the pathogenesis of IBD is still limited. In this review, we present recent information contributing to a better understanding of mechanisms underlying IBD.
Here, we attempt to highlight novel environmental triggers, data on the gut microbiota, its interaction with the host, and the potential influence of diet and food components. We discuss recent findings on defective signaling pathways and the potential effects on the immune response, and we present new data on epigenetic changes, inflammasome, and damage-associated molecular patterns associated with IBD.
The continuing identification of several epigenetic, transcriptomic, proteomic, and metabolomic alterations in patients with IBD reflects the complex nature of the disease and suggests the need for innovative approaches such as systems biology for identifying novel relevant targets in IBD.
克罗恩病和溃疡性结肠炎是炎症性肠病（IBD）的两种主要形式，是病因不明的慢性疾病，被视为典型的复杂疾病。尽管最近有诸多进展，但对IBD发病机制的全面认识仍然有限。在本综述中，我们介绍有助于更好理解IBD潜在机制的最新信息。
在此，我们试图强调新的环境触发因素、肠道微生物群的数据、其与宿主的相互作用以及饮食和食物成分的潜在影响。我们讨论信号通路缺陷的最新发现及其对免疫反应的潜在影响，并介绍与IBD相关的表观遗传变化、炎性小体和损伤相关分子模式的新数据。
在IBD患者中持续发现的几种表观遗传、转录组、蛋白质组和代谢组改变反映了该疾病的复杂性，并表明需要诸如系统生物学等创新方法来识别IBD中的新相关靶点。
