Figure 4.

Short‐term therapy with glucocorticoid modulates leucocyte responsiveness during colitis onset. C57BL/6 mice were exposed to dextran sulphate sodium (DSS) 3% and treated with dexamethasone as described in the Material and methods. The spleen was collected on the 6th day for immunophenotyping experiments. In (a) CD3⁺ CD4⁺ cells, (b) CD3⁺ CD8⁺ cells, (c) CD49b⁺ and (d) CD3⁺ CD49b⁺, evaluated by flow cytometry. Spleen cell function was evaluated by the frequency of CD4⁺ T cells producing (e) interferon‐γ (IFN‐γ), (f) interleukin‐17 (IL‐17), (g) IL‐4 and (h) IL‐10. The proliferation index (i) was determined by cytometry analysis of splenocytes from mice with colitis treated or not with glucocorticoids in vivo and cultured ex vivo in the absence or presence of concanavalin A (ConA). DSS: C57BL/6 mice exposed to DSS; DSS+GC: C57BL/6 mice exposed to DSS and treated with glucocorticoids. The dashed lines in (a–h) correspond to the group of C57BL/6 control mice not exposed to DSS and in (i) to the cells from these control mice cultured without re‐stimuli in vitro. These results are representative of three independent experiments with five mice/group. Data were analysed using one‐tailed unpaired t‐tests in (a), (b), (c), (d), (g) and Mann–Whitney one‐tailed tests in (e), (f), (h), (i). *P < 0·05.