title: A shift toward T helper 2 responses and an increase in modulators of innate immunity in depressed patients treated with escitalopram.
abstract: Depression is hypothesized to involve inflammatory processes, and identifying the key cytokines targeted by antidepressant drugs is critical for tailoring treatment to specific cases. However, investigating a limited number of cytokines at one time cannot provide a broad picture of antidepressant-associated immunomodulation. Cytokines act in a network where one could demonstrate pleiotropism, redundancy, synergy, and antagonism with other cytokine functions. This study was aimed at determining whether escitalopram functions as an anti-inflammatory agent and, if so, how it influences cytokine networks. A total of 24 healthy controls and 26 patients with clinical depression requiring inpatient treatment were recruited. A multiplex assay, an efficient tool to simultaneously measure 27 cytokines, was applied in patients with depression before and after 4-week escitalopram treatment. Healthy controls did not take escitalopram and completed cytokine analyses once. We demonstrated that escitalopram increased the levels of interleukin (IL)-1 receptor antagonist and IL-2. Moreover, escitalopram contributed to a shift toward T helper 2 responses and an increase in modulators of innate immunity, leading to a decrease of immune system activation, both innate and adaptive. We suggest that escitalopram modulates the balance of IL-1 and IL-1 receptor antagonist and improves the function and number of T regulatory cells. However, diverse conclusions could be drawn if only a few cytokines were assessed or different significance levels were used. Further studies should investigate a wide range of cytokines in a reliable and valid way, which is key to disentangling the effects of different antidepressants on inflammatory processes.
authors: Department of Psychiatry, Beitou Branch, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, ROC.
authors: Pei-Shen
authors: PS
authors: Ho
authors: Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan, ROC; Department of Psychiatry, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, ROC.
authors: Yi-Wei
authors: YW
authors: Yeh
authors: Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan, ROC; Department of Psychiatry, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, ROC.
authors: San-Yuan
authors: SY
authors: Huang
authors: Department of Psychiatry, Beitou Branch, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, ROC; Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan, ROC. Electronic address: lcsyfw@gmail.com.
authors: Chih-Sung
authors: CS
authors: Liang
mesh_terms: D000328:Adult; D000928:Antidepressive Agents / Q000494:pharmacology / Q000627:therapeutic use*; D016022:Case-Control Studies; D015283:Citalopram / Q000494:pharmacology / Q000627:therapeutic use*; D016207:Cytokines / Q000187:drug effects / Q000276:immunology*; D003866:Depressive Disorder / Q000188:drug therapy / Q000276:immunology; D003865:Major Depressive Disorder / Q000188:drug therapy* / Q000276:immunology; D019263:Dysthymic Disorder / Q000188:drug therapy* / Q000276:immunology; D005260:Female; D006801:Humans; D007113:Immunity, Innate / Q000187:drug effects / Q000276:immunology*; D008297:Male; D018418:Th2 Cells / Q000187:drug effects / Q000276:immunology*; D055815:Young Adult
chemical_list: D000928:Antidepressive Agents; D016207:Cytokines; D015283:Citalopram
keywords: Antidepressant; Cytokine; Depression; Escitalopram; Inflammation; Multiplex assay