Pharmacological reports : PR · 2013
Inhibition of 2,4-dinitrofluorobenzene-induced contact hypersensitivity reaction by antidepressant drugs.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Curzytek Katarzyna, Kubera Marta, Majewska-Szczepanik Monika, Szczepanik Marian, Marcińska Katarzyna, Ptak Włodzimierz, Duda Weronika, Leśkiewicz Monika, Basta-Kaim Agnieszka, Budziszewska Bogusława, Lasoń Władysław, Maes Michael
Аннотация
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)1-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 [(3)H]-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 Tc1 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)-γ 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 Tc1-dependent reactivity to DNFB is significantly suppressed by antidepressant drugs, which suggests their inhibitory effect on Tc1 mediated immunity.
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 [(3)H]-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 Tc1 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)-γ 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 Tc1-dependent reactivity to DNFB is significantly suppressed by antidepressant drugs, which suggests their inhibitory effect on Tc1 mediated immunity.