Inhibition of 2,4-dinitrofluorobenzene-induced contact hypersensitivity reaction by antidepressant drugs

Background: Contact hypersensitivity (CHS) induced by a topical application of hapten 2,4-dinitrofluorobenzene (DNFB), is a T cytotoxic (Tc)1-cell-mediated antigen-specific type of skin inflammation. Recently, it has been shown that antidepressant drugs inhibit the T helper (Th)l-mediated CHS reaction induced by picryl chloride. The aim of present study was to establish the effect of two-week desipramine or fluoxetine administration on the CHS reaction induced by DNFB. Methods: Balb/c (H-2(d)) male mice were divided into six groups: 1) vehicle-treated negative control group; 2) desipramine-treated negative control group; 3) fluoxetine-treated negative control group; 4) vehicle-treated DNFB group (positive control group); 5) desipramine-treated DNFB group; 6) fluoxetine-treated DNFB group. T lymphocytes proliferation was determined by incorporation of [H-3]-thymidine to DNA of concanavalin A stimulated cells. ELISA test was used for estimation of cytokines production. Results: The antidepressants significantly suppressed the CHS reaction mediated by Tcl cells: desipramine by 55% and fluoxetine by 54% compared to the positive control. Moreover, the antidepressants decreased the proliferative activity of splenocytes and the ability of splenocytes to produce interleukin (IL)-6 and interferon (IFN)-gamma and increased IL-10 production by the lymph node (LN) cells of DNFB-treated mice. Conclusion: The results of the present study show that the Tcl-dependent reactivity to DNFB is significantly suppressed by antidepressant drugs, which suggests their inhibitory effect on Tcl mediated immunity.