single-cell RNA-seq data with annotations (mouse with ulcerative colitis, 85,000 cells)

Ulcerative colitis, a prominent form of inflammatory bowel disease, is a complex disease caused by a dysregulated immune reaction against commensal microbes residing in the host. Despite considerable progress in comprehending host transcriptomics, gaps persist in our understanding of immune metabolic alterations specific to ulcerative colitis. Utilizing comprehensive single-cell RNA-seq and microbial analysis, we characterized distinct cell clusters in the mouse colon at different time points following dextran sodium sulfate induction. 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 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.