Objective：To investigate the effect of loss of aryl hydrocarbon receptor（AhR） on intestinal inflammation and its potential mechanism. Methods：Mice were assigned into 4 groups：wild type control group（WT control），wild type colitis group（WT TNBS），AhR knockout control group（AhR-/- control） and AhR knockout colitis group（AhR-/- TNBS）. Acute experimental colitis was established using 2，4，6-trinitrobenzenesulfonic acid（TNBS）. Disease activity index（DAI）score，colon length and histological score were compared among different groups. The expression of regulatory T cell（Treg） specific transcription factor FoxP3 was measured by Western blot（WB） and immunofluorescence（IF）. Proportion of Treg cells in peripheral blood was detected by flow cytometry. Results：Compared with WT mice，AhR-/- mice experienced much more severe colitis after TNBS administration，manifested by more weight loss（P < 0.01），severe diarrhea and bloody stool，higher DAI score（P < 0.001），shorter colon length（P < 0.01） and poorer histological findings（P < 0.001）. Also，expression of FoxP3 in the colon and proportion of Treg cells in peripheral blood were much lower in AhR-/- TNBS mice（P < 0.01）. Conclusion：Deletion of AhR was found to aggravate experimental colitis. This effect could be associated with the decrease of Treg cells in the colon and peripheral blood.