GSE168053
Transcriptome profiling of DSS-induced colonic and anal inflammation and injury in mice
Oral administration of dextran sulfate sodium (DSS) to mice induces ulceration and inflammation in the colons of mice. These changes are somewhat similar to those seen in human inflammatory bowel disease. Here we provide a full transcriptome (RNA-Seq) analysis of different gastrointestinal tissues in the regions affected by the DSS chemical, at different timepoints during the injury-inflammation-recovery cycle. The profiled regions include the distal colon (rectum), where the histological changes are most pronounced, the mid-colon, the anus, which is relatively resistant to damage, and the squamous neo-epithelium of the colon, a skin-like tissue that is found in the colon and is believed to be associated with wound healing. We find that administration of DSS is associated with upregulation of cytokines and inflammatory markers. Moreover, stem cell markers of the homeostatic colonic epithelium are depleted, consistent with reprogramming of epithelia to adopt a wound-healing phenotype. Thus, this dataset faithfully recovers broad changes in gene expression in a mouse model of inflammatory bowel disease-like damage. Overall design: Wildtype C57Bl/6 mice were exposed to the DSS colitis model for 6 d, beginning on experimental day (exp d) 0. They were dissected and their anorectal junctions analyzed via single-cell RNA-Seq at experimental day (exp d) 0 (unchallenged mice), exp d 7 (highly colitic mice), and exp d 42 (recovered mice). On either exp d 0 (uninjured controls), 3, 6, 9, 14, or 20, mice were dissected and their distal gastrointestinal tracts isolated. The tissue was divided into mid-colonic ("prox"), rectal ("dist"), anal ("anal"), and squamous neo-epithelial ("meta") sections for transcriptome profiling using RNA-Seq. In each tissue section, the muscle layer was dissected out and discarded prior to RNA isolation.