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Effect of desipramine on immunological parameters in mice, and their reversal by stress
M Kubera1, V Holan, A Basta-Kaim
1Department of Immunobiology, Institute of Pharmacology, Polish Academy of Sciences, Krakow.
Immunomodulation of cell-mediated immunity is demonstrated in mice, after administration of desipramine, a noradrenaline-reuptake inhibitor, with or without exposing the mice later to an acute swimming stress. A single i.p. injection of 10 mg/kg desipramine to naive mice increased the relative weight of their spleens, the response of their splenocytes to the mitogen concavaline-A and their ability to produce IL-10, as compared to saline controls. Exposing the desipramine-treated mice to a swimming stress significantly reduced these parameters, as well as the levels of IL-2 and IFN-gamma, as compared to desipramine-treated mice. Stress alone reduced the weight of the spleen, and the ability of splenocytes to produce IFN-gamma. As desipramine and acute stress have stimulatory effect on the sympathetic system, it is suggested that a concomitant administration of the drug and a stressful event of these mice, change the splenocytes' micro-environment of sympathetic transmitters, and inhibit their function. These results may be partially due to impairment in the T-helper cell function by a beta-adrenoreceptor-dependent mechanism.
Immunomodulation of cell-mediated immunity is demonstrated in mice, after administration of desipramine, a noradrenaline-reuptake inhibitor, with or without exposing the mice later to an acute swimming stress. A single i.p. injection of 10 mg/kg desipramine to naive mice increased the relative weight of their spleens, the response of their splenocytes to the mitogen concavaline-A and their ability to produce IL-10, as compared to saline controls. Exposing the desipramine-treated mice to a swimming stress significantly reduced these parameters, as well as the levels of IL-2 and IFN-gamma, as compared to desipramine-treated mice. Stress alone reduced the weight of the spleen, and the ability of splenocytes to produce IFN-gamma. As desipramine and acute stress have stimulatory effect on the sympathetic system, it is suggested that a concomitant administration of the drug and a stressful event of these mice, change the splenocytes' micro-environment of sympathetic transmitters, and inhibit their function. These results may be partially due to impairment in the T-helper cell function by a beta-adrenoreceptor-dependent mechanism.