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
{"title":"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","authors":"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","doi":"10.1101/2024.08.14.607902","DOIUrl":null,"url":null,"abstract":"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.","PeriodicalId":501213,"journal":{"name":"bioRxiv - Systems Biology","volume":"7 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Integrated multi-model analysis of intestinal inflammation exposes key molecular features of preclinical and clinical IBD\",\"authors\":\"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\",\"doi\":\"10.1101/2024.08.14.607902\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"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.\",\"PeriodicalId\":501213,\"journal\":{\"name\":\"bioRxiv - Systems Biology\",\"volume\":\"7 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-09-13\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"bioRxiv - Systems Biology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1101/2024.08.14.607902\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"bioRxiv - Systems Biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1101/2024.08.14.607902","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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.