Amelioration of experimental colitis after short-term therapy with glucocorticoid and its relationship to the induction of different regulatory markers.

摘要: The clinical benefits of short-term therapy with glucocorticoids (GC) in patients inflammatory bowel disease (IBD) are widely known. However, the effects this treatment towards re-establishment regulatory network IBD not fully explored. We have evaluated immunological abbreviated GC experimental colitis induced by 3% dextran sulphate sodium C57BL/6 mice. Treatment improved outcome, constrained circulating leucocytes and ameliorated intestinal inflammation. control local responses involved a reduction expression interferon-γ interleukin-1β, associated augmented mRNA levels peroxisome proliferator-activated receptors (α γ) intestine. Furthermore, there was CD4+ T cells producing interferon-γ, together an increased frequency putative population interleukin-10, spleen. These systemic alterations were accompanied decrease proliferative potential splenocytes mice treated vivo GC. Notably, also led to increase markers GITR, CTLA-4, PD-1, CD73 FoxP3, more prominently Taken together, our results pointed role leucocyte responsiveness system, which probably contributed restoration immune balance. Finally, is first time that modulation broad number model colitis.