Colitis promotes neuronal differentiation of Sox2+ and PLP1+ enteric cells.

摘要: Mechanisms mediating adult enteric neurogenesis are largely unknown. Using inflammation-associated models and a transgenic approach, we aimed to understand the cell-source for new neurons in infectious inflammatory colitis. Dextran sodium sulfate (DSS) Citrobacter rodentium colitis (CC) was induced mice colonic were quantified. Sox2GFP PLP1GFP confirmed cell-type specificity of these markers. Sox2CreER:YFP PLP1creER:tdT used determine fate cells after Sox2 expression investigated human patients with Clostridium difficile or ulcerative Both DSS CC led increased neurons. Following mice, YFP initially expressed predominantly by glia becomes following colitis, without observable DNA replication. Similarly PLP1CreER:tdT PLP1 that co-express S100b but not RET also give rise In Sox2-expressing increase from 1–2% an average 14% The express calretinin, thus appear be excitatory. These results suggest promotes rapid humans through differentiation Sox2- PLP1-expressing cells, which represent and/or neural progenitors. Further defining will improve understanding treatment injury-associated intestinal motility/sensory disorders.