Systems biology approach highlights mechanistic differences between Crohn’s disease and ulcerative colitis

Abstract The molecular mechanisms of IBD have been the subject of intensive exploration. We, therefore, assembled the available information into a suite of causal biological network models, which offer comprehensive visualization of the processes underlying IBD. Scientific text was curated by using...

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Autores principales:	Pedro A. Ruiz Castro, Hasmik Yepiskoposyan, Sylvain Gubian, Florian Calvino-Martin, Ulrike Kogel, Kasper Renggli, Manuel C. Peitsch, Julia Hoeng, Marja Talikka
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/5020808525844ce6a5169f204e832fcc
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spelling	oai:doaj.org-article:5020808525844ce6a5169f204e832fcc2021-12-02T17:50:41ZSystems biology approach highlights mechanistic differences between Crohn’s disease and ulcerative colitis10.1038/s41598-021-91124-32045-2322https://doaj.org/article/5020808525844ce6a5169f204e832fcc2021-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-91124-3https://doaj.org/toc/2045-2322Abstract The molecular mechanisms of IBD have been the subject of intensive exploration. We, therefore, assembled the available information into a suite of causal biological network models, which offer comprehensive visualization of the processes underlying IBD. Scientific text was curated by using Biological Expression Language (BEL) and compiled with OpenBEL 3.0.0. Network properties were analysed by Cytoscape. Network perturbation amplitudes were computed to score the network models with transcriptomic data from public data repositories. The IBD network model suite consists of three independent models that represent signalling pathways that contribute to IBD. In the “intestinal permeability” model, programmed cell death factors were downregulated in CD and upregulated in UC. In the “inflammation” model, PPARG, IL6, and IFN-associated pathways were prominent regulatory factors in both diseases. In the “wound healing” model, factors promoting wound healing were upregulated in CD and downregulated in UC. Scoring of publicly available transcriptomic datasets onto these network models demonstrated that the IBD models capture the perturbation in each dataset accurately. The IBD network model suite can provide better mechanistic insights of the transcriptional changes in IBD and constitutes a valuable tool in personalized medicine to further understand individual drug responses in IBD.Pedro A. Ruiz CastroHasmik YepiskoposyanSylvain GubianFlorian Calvino-MartinUlrike KogelKasper RenggliManuel C. PeitschJulia HoengMarja TalikkaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-14 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Pedro A. Ruiz Castro Hasmik Yepiskoposyan Sylvain Gubian Florian Calvino-Martin Ulrike Kogel Kasper Renggli Manuel C. Peitsch Julia Hoeng Marja Talikka Systems biology approach highlights mechanistic differences between Crohn’s disease and ulcerative colitis
description	Abstract The molecular mechanisms of IBD have been the subject of intensive exploration. We, therefore, assembled the available information into a suite of causal biological network models, which offer comprehensive visualization of the processes underlying IBD. Scientific text was curated by using Biological Expression Language (BEL) and compiled with OpenBEL 3.0.0. Network properties were analysed by Cytoscape. Network perturbation amplitudes were computed to score the network models with transcriptomic data from public data repositories. The IBD network model suite consists of three independent models that represent signalling pathways that contribute to IBD. In the “intestinal permeability” model, programmed cell death factors were downregulated in CD and upregulated in UC. In the “inflammation” model, PPARG, IL6, and IFN-associated pathways were prominent regulatory factors in both diseases. In the “wound healing” model, factors promoting wound healing were upregulated in CD and downregulated in UC. Scoring of publicly available transcriptomic datasets onto these network models demonstrated that the IBD models capture the perturbation in each dataset accurately. The IBD network model suite can provide better mechanistic insights of the transcriptional changes in IBD and constitutes a valuable tool in personalized medicine to further understand individual drug responses in IBD.
format	article
author	Pedro A. Ruiz Castro Hasmik Yepiskoposyan Sylvain Gubian Florian Calvino-Martin Ulrike Kogel Kasper Renggli Manuel C. Peitsch Julia Hoeng Marja Talikka
author_facet	Pedro A. Ruiz Castro Hasmik Yepiskoposyan Sylvain Gubian Florian Calvino-Martin Ulrike Kogel Kasper Renggli Manuel C. Peitsch Julia Hoeng Marja Talikka
author_sort	Pedro A. Ruiz Castro
title	Systems biology approach highlights mechanistic differences between Crohn’s disease and ulcerative colitis
title_short	Systems biology approach highlights mechanistic differences between Crohn’s disease and ulcerative colitis
title_full	Systems biology approach highlights mechanistic differences between Crohn’s disease and ulcerative colitis
title_fullStr	Systems biology approach highlights mechanistic differences between Crohn’s disease and ulcerative colitis
title_full_unstemmed	Systems biology approach highlights mechanistic differences between Crohn’s disease and ulcerative colitis
title_sort	systems biology approach highlights mechanistic differences between crohn’s disease and ulcerative colitis
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/5020808525844ce6a5169f204e832fcc
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Systems biology approach highlights mechanistic differences between Crohn’s disease and ulcerative colitis

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