Inhibitory effect of antidepressant drugs on contact hypersensitivity reaction.
BACKGROUND
Contact hypersensitivity (CS) reaction in the skin is T-cell mediated immune reaction which plays a major role in the pathogenesis and chronicity of various inflammatory skin disorders and, like other delayed-type hypersensitivity (DTH) reactions, affords immunity against tumor cells and microbes. CS response is a self-limiting reaction, and interleukin (IL)-10 is considered to be a natural suppressant of cutaneous inflammatory response. Recently, it has been demonstrated that major depression is related to activation of the inflammatory response and elevation of some parameters of cell-mediated immunity. It has been suggested that such activation of the immune system may play a role in etiology of depression. If this immunoactivation is involved in etiology of depression, one would expect that antidepressant agents may have negative immunoregulatory effects. To the best of our knowledge, the effect of antidepressants on contact hypersensitivity has not been studied.


METHODS
The aim of the present study was to establish the effect of prolonged desipramine or fluoxetine treatment on CS reaction to picryl chloride.


RESULTS
Antidepressants significantly suppressed CS reaction, fluoxetine by 53% whereas desipramine by 47% compared to positive control. Moreover, desipramine and fluoxetine decreased relative weight of auxillary lymph nodes. Desipramine decreased also relative weight of inguinal lymph nodes and spleens whereas desipramine and fluoxetine increased production of IL-10 in comparison to positive control.


CONCLUSIONS
The observed effect of antidepressant drugs on CS reaction is consistent with the hypothesis that T-cell mediated immunity is targeted by antidepressants.
Department of Experimental Neuroendocrinology, Institute of Pharmacology, Polish Academy of Sciences, Smętna 12, PL 31-343 Kraków, Poland. kubera@if-pan.krakow.pl
Marta
M
Kubera
Katarzyna
K
Curzytek
Monika
M
Majewska-Szczepanik
Marian
M
Szczepanik
Katarzyna
K
Marcińska
Włodzimierz
W
Ptak
Monika
M
Leśkiewicz
Michael
M
Maes
Agnieszka
A
Basta-Kaim
Bogusława
B
Budziszewska
Jan
J
Detka
Weronika
W
Duda
Władysław
W
Lasoń
D000818:Animals; D018687:Antidepressive Agents, Second-Generation / Q000008:administration & dosage / Q000494:pharmacology; D000929:Antidepressive Agents, Tricyclic / Q000008:administration & dosage / Q000494:pharmacology; D003877:Dermatitis, Contact / Q000188:drug therapy* / Q000209:etiology / Q000276:immunology; D003891:Desipramine / Q000008:administration & dosage / Q000494:pharmacology*; D005473:Fluoxetine / Q000008:administration & dosage / Q000494:pharmacology*; D016753:Interleukin-10 / Q000096:biosynthesis; D008198:Lymph Nodes / Q000187:drug effects / Q000378:metabolism; D051379:Mice; D008808:Mice, Inbred CBA; D009929:Organ Size / Q000187:drug effects; D010853:Picryl Chloride / Q000633:toxicity*; D013154:Spleen / Q000187:drug effects / Q000378:metabolism; D013601:T-Lymphocytes / Q000276:immunology
D018687:Antidepressive Agents, Second-Generation; D000929:Antidepressive Agents, Tricyclic; D005473:Fluoxetine; D016753:Interleukin-10; D003891:Desipramine; D010853:Picryl Chloride