Fiocchi Claudio
Department of Gastroenterology and Hepatology, Digestive Disease Institute, and Department of Pathobiology, Lerner Research Institute, The Cleveland Clinic Foundation, Cleveland, Ohio, USA.
Dig Dis. 2014;32 Suppl 1:96-102. doi: 10.1159/000367836. Epub 2014 Dec 17.
The complexity of IBD is well recognized as are the putative four major components of its pathogenesis, i.e. environment, genetic makeup, gut microbiota and mucosal immune response. Each of these components is extremely complex on its own, and at present should be more appropriately defined by the terms 'exposome', 'genome', 'microbiome' and 'immunome', respectively, based on the 'ome' suffix that refers to a totality of some sort. None of these 'omes' is apparently capable of causing IBD by itself; it is instead the intricate and reciprocal interaction among them, through the so-called 'IBD interactome', that results in the emergence of IBD, or more appropriately the 'IBD integrome'. To deal with and understand such overwhelming biological complexity, new approaches and tools are needed, and these are represented by 'omics', defined as the study of related sets of biological molecules in a comprehensive fashion, such as genomics, transcriptomics, proteomics, metabolomics, and so on. Numerous bioinformatics-based tools are available to explore and take advantage of the massive amount of information that can be generated by the analysis of the various omes and their interactions, aiming at identifying the molecular interactome underlying any particular status of health and disease. These novel approaches are fully applicable to IBD and allow us to achieve the ultimate goal of developing and applying personalized medicine and far more effective therapies to individual patients with Crohn's disease and ulcerative colitis. For the practicing gastroenterologist, an omics-based delivery of healthcare may be intimidating, but it must be accepted and implemented if he or she is to provide the best possible care to IBD patients.
炎症性肠病(IBD)的复杂性已得到充分认识,其发病机制的四个主要推定组成部分也是如此,即环境、基因构成、肠道微生物群和黏膜免疫反应。这些组成部分中的每一个本身都极其复杂,目前分别用“暴露组”“基因组”“微生物组”和“免疫组”来更恰当地定义,这些术语都基于“组”这个后缀,它表示某种整体。显然,这些“组”中没有一个能够单独引发IBD;相反,正是它们之间通过所谓的“IBD相互作用组”进行的复杂且相互的相互作用,导致了IBD的出现,或者更恰当地说是“IBD整合组”的出现。为了应对和理解这种压倒性的生物学复杂性,需要新的方法和工具,这些方法和工具由“组学”来代表,“组学”被定义为以全面的方式研究相关生物分子集,如基因组学、转录组学、蛋白质组学、代谢组学等等。有许多基于生物信息学的工具可用于探索和利用通过分析各种“组”及其相互作用而产生的大量信息,旨在识别任何特定健康和疾病状态背后的分子相互作用组。这些新方法完全适用于IBD,并使我们能够实现为克罗恩病和溃疡性结肠炎患者开发和应用个性化医学以及更有效疗法的最终目标。对于执业胃肠病学家来说,基于组学的医疗服务可能令人生畏,但如果他或她要为IBD患者提供尽可能好的护理,就必须接受并实施。
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