Crohn's disease (CD) and ulcerative colitis (UC) are the two main forms of inflammatory bowel disease (IBD). Previous studies reported increased levels of proteolytic activity in stool and tissue samples from IBD patients, while the reestablishment of the proteolytic balance abrogates the development of experimental colitis. Furthermore, recent data suggest that IBD occurs in genetically predisposed individuals who develop an abnormal immune response to intestinal microbes once exposed to environmental triggers. In this review, we highlight the role of proteases in IBD pathophysiology, we showcase how the main cellular pathways associated with IBD influences proteolytic unbalance and how functional proteomics are allowing the unambiguous identification of dysregulated proteases in IBD, paving the way to the development of new protease inhibitors as a new potential treatment.

中文翻译：

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炎症性肠病的病理生理中遗传危险因素与蛋白水解失调之间的相互作用。

克罗恩病（CD）和溃疡性结肠炎（UC）是炎性肠病（IBD）的两种主要形式。先前的研究报道了来自IBD患者的粪便和组织样品中蛋白水解活性水平的提高，而蛋白水解平衡的重建消除了实验性结肠炎的发展。此外，最新数据表明，IBD发生在遗传易感人群中，一旦暴露于环境触发因素，这些个体会对肠道微生物产生异常的免疫反应。在本文中，我们重点介绍了蛋白酶在IBD病理生理中的作用，展示了与IBD相关的主要细胞途径如何影响蛋白水解失衡，以及功能蛋白质组学如何明确鉴定IBD中失调的蛋白酶，