BioProject

In this study, we attempted to dissect the dynamic changes during inflammation using well-prepared scRNA-seq dataset. More...

In this study, we attempted to dissect the dynamic changes during inflammation using well-prepared scRNA-seq dataset. Specifically, we tried to characterize the pathology and the biological mechanism underlying the ulcerative colitis separately for the acute and chronic colitis. We observed a significant reduction in epithelial populations during acute colitis, indicating tissue damage, with a partial recovery observed in chronic inflammation. Analyses of cell-cell interactions demonstrated shifts in networking patterns among different cell types during disease progression. Notably, macrophage phenotypes exhibited diversity, with a pronounced polarization towards the pro-inflammatory M1 phenotype in chronic condition, suggesting the role of macrophage heterogeneity in disease progression. Analysis of the intestinal microbiome revealed significant alterations in composition and metabolism pathways, particularly the nicotinamide pathway. Additionally, dysbiosis was linked to dysregulation of NAD homeostasis through NAMPT, providing insights into potential therapeutic strategies. The study also highlighted the role of T cell differentiation in the context of dysbiosis and its implications in colitis progression, emphasizing the need for targeted interventions to modulate the inflammatory response and immune balance in colitis. Overall design: We conducted single-cell RNA sequencing (scRNA-Seq) using Chromium (10X Genomics) on samples from 3 healthy mouse colons, 3 mouse colons with acute colitis induced by DSS, and 4 mouse colons with chronic colitis induced by DSS. Less...