Mitochondrial translocator protein deficiency exacerbates pathology in acute experimental ulcerative colitis.

In human patients and animal models of ulcerative colitis (UC), upregulation of the mitochondrial translocator protein (TSPO) in the colon is consistent with inflammation. Although the molecular function for TSPO remains unclear, it has been investigated as a therapeutic target for ameliorating UC pathology. In this study, we examined the susceptibility of gene-deleted ( ) mice to insults as provided by the dextran sodium sulfate (DSS)-induced acute UC model.