Impaired T-cell dependent humoral response and its relationship with T lymphocyte sensitivity to stress hormones in a chronic mild stress model of depression.

The humoral response and the role of catecholamines and corticosterone were analyzed in a chronic mild stress (CMS) model of depression. Mice subjected for more than 6 weeks to CMS showed a significant decrease in T-cell dependent antibody production. However, T-cell independent humoral response was not altered. Serum corticosterone levels and splenic norepinephrine (NE) contents showed an early increase but they were not altered after prolonged CMS exposure. Nevertheless, hormonal inhibitory effect on T lymphocyte reactivity was higher in 6-week CMS mice compared to non-exposed animals. Thus, our results suggest that the impaired T-cell dependent humoral response in a CMS model of depression is neither related to changes in glucocorticoids nor in NE levels but is correlated with an increment of T-cell sensitivity to stress hormones. These findings would underlie the involvement of catecholamines and glucocorticoid lymphocyte receptors in the immune alterations observed in stress and depression.

Fluoxetine action upon human T lymphocyte proliferation.

The purpose of this study was to analyze the effect of fluoxetine upon human T lymphocyte proliferation, and to assess the early signals elicited after T cell triggering and cAMP formation. Blood samples from normal human volunteers were drawn from venipuncture and T cells were cultured in the presence or absence of Concanavalin A (Con A) and fluoxetine. Protein Kinase C (PKC) levels and cyclic adenosine monophosphate (cAMP) formation were also measured. Fluoxetine exerted dual effect, depending on the degree of lymphocyte activation: at mitogenic concentrations of Con A (2 micrograms/ml), we observed an inhibitory effect on cellular proliferation. This inhibitory effect involves PKC degradation and cAMP formation. On the other hand, when submitogenic Con A concentrations (1 microgram/ml) were used, fluoxetine stimulated the cellular response and increased PKC translocation. The participation of extracellular calcium mobilization could be involved in these mechanisms. According to our results, fluoxetine seems to modulate calcium influx which, in turn, would influence PKC translocation, thus modulating the immune response through a mechanism that could be involving cAMP participation.

Fluoxetine action upon human T lymphocyte proliferation

The purpose of this study was to analyze the effect of fluoxetine upon human T lymphocyte proliferation, and to assess the early signals elicited after T cell triggering and cAMP formation. Blood samples from normal human volunteers were drawn from venipuncture and T cells were cultured in the presence or absence of Concanavalin A (Con A) and fluoxetine. Protein Kinase C (PKC) levels and cyclic adenosine monophosphate (cAMP) formation were also measured. Fluoxetine exerted dual effect, depending on the degree of lymphocyte activation: at mitogenic concentrations of Con A (2 mug/ml), we observed na inhibitory effect on cellular proliferation. This inhibitory effect involves PKC degradation and cAMP formation. On the other hand, when submitogenic Con A concentrations (1mug/ml) were used, fluoxetine stimulated the cellular response and increased PKC traslocation. The participation of extracellular calcium mobilization could be involved in these mechanisms. According to our results, fluoxetine seems to modulate calcium influx which, in turn, would influence PKC traslocation, thus modulating the immune response through a mechanism that could be involving cAMP participation. (AU)

Fluoxetine action upon human T lymphocyte proliferation

The purpose of this study was to analyze the effect of fluoxetine upon human T lymphocyte proliferation, and to assess the early signals elicited after T cell triggering and cAMP formation. Blood samples from normal human volunteers were drawn from venipuncture and T cells were cultured in the presence or absence of Concanavalin A (Con A) and fluoxetine. Protein Kinase C (PKC) levels and cyclic adenosine monophosphate (cAMP) formation were also measured. Fluoxetine exerted dual effect, depending on the degree of lymphocyte activation: at mitogenic concentrations of Con A (2 mug/ml), we observed na inhibitory effect on cellular proliferation. This inhibitory effect involves PKC degradation and cAMP formation. On the other hand, when submitogenic Con A concentrations (1mug/ml) were used, fluoxetine stimulated the cellular response and increased PKC traslocation. The participation of extracellular calcium mobilization could be involved in these mechanisms. According to our results, fluoxetine seems to modulate calcium influx which, in turn, would influence PKC traslocation, thus modulating the immune response through a mechanism that could be involving cAMP participation.