Lastly, we identified a cluster of stress-related genes, including activator protein 1 components JUNB and ATF3, as significantly upregulated in active UC but not in CD, revealing an interesting aspect of IBD heterogeneity. We also see an epithelial downregulation of retinoic acid-responsive nuclear receptors ( RARA, RARB, RXRA), but upregulation of retinoid-metabolizing enzymes ( RDH11, ALDH1A2, ALDH1A3), which together suggest a perturbation of epithelial vitamin A signaling during active IBD. HLA-DPA1, HLA-DPB1, HLA-DRA) and key transcription factors/activators ( STAT1, IRF1, CIITA). Our data show a distinct upregulation of the antigen presentation machinery during inflammation, including major histocompatibility complex class II molecules (e.g. Weighted gene co-expression network analysis was used to stratify genes into modules, which were subsequently characterized using enrichment analysis. The analysis identified 3706 genes as differentially expressed between active IBD epithelium and HC. By using laser capture microdissection (LCM) coupled with RNA sequencing, we aimed to characterize the expressional changes of the isolated colonic epithelial monolayer from ulcerative colitis (UC) and Crohn’s disease (CD) patients compared to healthy controls (HC). The majority of gene expression studies of IBD are generated from heterogeneous biopsies, providing no distinction between immune cells, the epithelium and other mucosal cells. In recent years it has become apparent that the epithelium is highly involved in inflammatory bowel disease (IBD) pathophysiology.

One minute cure for colitis