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Induced organoids derived from patients with ulcerative colitis recapitulate the colitic reactivity

ABSTRACT: We report the application of single nucleus RNA-seq technology for transcriptomic-wide profiling of the induced organoids derived from patients with ulcerative colitis (iHUCO) and normal induced organoids derived from the healthy colon (iHNO), along with their parental fibroblasts. By comapring the nucleus profiles of both iHUCOs and their parental fibroblasts (UC FBs) to iHNOs and normal fibroblasts (NL FBs), we found unique signatures exclusive to the UC samples but not the controls. We also report that UC FBs and iHUCOs share the layers of similarities in their single nucleus profile. This study provides a framework for the application of the induced patient-derived organoids as a more comprehensive model to study human UC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE152999 | GEO | 2020/10/09

REPOSITORIES: GEO

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Project description:Objective: Ulcerative colitis (UC) is a chronic disease with rising incidence and unclear etiology. The application of mass spectrometry-based post-genomic analysis methods shall support the development of molecular biomarker signatures providing status information with regard to UC pathomechanisms. Design: Pathomechanisms characteristic for UC were assessed by proteome profiling of human tissue specimen, obtained from five distinct colon locations each of 12 patients. Systemic disease-associated alterations were investigated by mass spectrometry-based multi-omics analyses comprising proteins, metabolites and eicosanoids of plasma obtained from UC patients during disease and upon remission in comparison to healthy controls. Results: Proteome profiling results identified colitis-associated activation of neutrophils, macrophages, B- and T-cells, platelets, fibroblasts and endothelial cells and indicated hypoxic stress, as well as a general reduction of mitochondrial proteins accompanying the establishment of apparent healing-promoting activities as well as scar formation. While the immune cells mainly contributed pro-inflammatory proteins, the colitis-associated epithelial cells, fibroblasts, endothelial cells and platelets predominantly formed anti-inflammatory and healing-promoting proteins. Blood plasma proteomics indicated chronic inflammation and platelet activation, whereas plasma metabolomics identified disease-associated deregulation of bile acids, eicosanoids and gut microbiome-derived metabolites. Upon remission, several, but not all, molecular candidate biomarker levels recovered to normal levels. These findings may indicate that pathomechanisms related to gut functions, gut microbiome status, microvascular damage and metabolic dysregulation associated with hypoxia may do not resolve uniformly upon remission. Conclusions: The establishment of disease-associated biomarker profiles related to molecular UC pathomechanisms may support the establishment of bioassays with improved prognostic power aiding individualized therapy.

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Induced organoids derived from patients with ulcerative colitis recapitulate the colitic reactivity

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