The majority of patients with depression are treated with antidepressant drugs that are in the serotonin reuptake inhibitor (SSRI) group. Different studies have been conducted on the effect of treatment with antidepressants on the level of pro-inflammatory cytokines. There have been studies on the effects of escitalopram, an SSRI group antidepressant, on the pro-inflammatory cytokine levels both in vivo and in vitro. The results of these studies do not overlap and therefore the escitalopram's effect on the immune system should be studied in more depth. In this study, we aimed to examine, in detail, the cytokine production amount by escitalopram treatment of the J774.2 macrophage cells and its intracellular mechanism of action by examining the PI3K and p38 pathways. As a result of our study, we observed that Escitalopram caused a significant increase in TNF-α, IL-6, and GM-CSF levels in mammalian macrophage cells, but did not induce IL-12p40 production. We observed that the p38 and PI3K pathways play a role in inflammation in the presence of Escitalopram.
Keywords: Cytokine; Escitalopram; Inflammation; Macrophage; P38; PI3K.
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