对肠道炎症的多模型综合分析揭示了临床前和临床 IBD 的关键分子特征

Miguel Gonzalez Acera, Jay V Patankar, Lena Erkert, Roodline Cineus, Reyes Gamez Belmonte, Tamara Leupold, Marvin Bubeck, Li-li Bao, Martin Dinkel, Ru Wang, Heidi Limberger, Iris Stolzer, Katharina Gerlach, Fabrizio Mascia, Kristina Koop, Christina Plattner, Gregor Sturm, Benno Weigmann, Claudia Guenther, Stefan Wirtz, Kai Hildner, Anja A Kuehl, Britta Siegmund, Raja Atreya, The IBDome Consortium, Ahmed N Hegazy, Zlatko Trajanoski, Markus F Neurath, Christoph Becker
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引用次数: 0

摘要

炎症性肠病(IBD)是一种慢性肠道炎症,发病机制复杂多样。虽然有各种动物模型可用于研究与人类 IBD 相关的特定疾病机制,但目前还缺乏一个将这些动物模型与 IBD 病理生理学联系起来的综合比较框架。在本研究中,我们提供了一个框架,该框架采用基于卷宗和统计相关性分析的方法,描述了 13 种广泛使用的小鼠模型在转录组水平上遇到的共同和独特特征。我们对小鼠模型与已建立的以及新的患者数据集进行的转录组比较分析揭示了 IBD 的特定疾病机制。此外,我们还发现了小鼠模型与患者队列之间具有可比性的 IBD 相关通路、本体和细胞过程。我们的研究结果为选择最合适的实验范式来模拟 IBD 发病机制的独特特征提供了宝贵的资源,从而可以在组织、细胞和亚细胞水平上进行分析。
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Integrated multi-model analysis of intestinal inflammation exposes key molecular features of preclinical and clinical IBD
Inflammatory bowel disease (IBD) is a chronic inflammatory condition of the intestine with a complex and multifaceted pathogenesis. While various animal models exist to study specific disease mechanisms relevant to human IBD, a comprehensive comparative framework linking these to IBD pathophysiology is lacking. In this study, we provide a framework that delineates common and unique features encountered at the transcriptomic level in 13 widely used mouse models, employing both curation-based and statistically correlative analyses. Our comparative transcriptomic analyses between mouse models versus established as well as new patient datasets reveal specific disease mechanisms in IBD. Furthermore, we identify IBD-related pathways, ontologies, and cellular processes that are comparable between mouse models and patient cohorts. Our findings provide a valuable resource for selecting the most appropriate experimental paradigm to model unique features of IBD pathogenesis, allowing analysis at the tissue, cellular, and subcellular levels.
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