کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6819158 | 547401 | 2015 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
A shift toward T helper 2 responses and an increase in modulators of innate immunity in depressed patients treated with escitalopram
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کلمات کلیدی
5-HTSSRIsIFN-γIL-1RAGM-CSFHDRSMCP-15-hydroxytryptamineFGFPDGFIP-10MIP-1αT helperMultiplex assay - آزمایش چندتاییinterleukin-1 receptor antagonist - آنتاگونیست گیرنده اینترلوکین-1Depression - افسردگیinflammation - التهاب( توروم) interleukin-1 - اینترلوکین-1ELISA - تست الیزاEnzyme-linked immunosorbent assay - تست الیزاtumor necrosis factor alpha - تومور نکروز عامل آلفاCytokine - سیتوکینAntidepressant - ضدافسردگیgranulocyte-macrophage colony-stimulating factor - عامل گرانولوسیت-ماکروفاژ colony-stimulating factorgranulocyte colony-stimulating factor - فاکتور تحریک کننده کلنی گرانولوسیتVascular endothelial growth factor - فاکتور رشد اندوتلیال عروقیVascular Endothelial Growth Factor (VEGF) - فاکتور رشد اندوتلیال عروقی (VEGF)platelet-derived growth factor - فاکتور رشد حاصل از پلاکتfibroblast growth factor - فاکتور رشد فیبروبلاستG-CSF - فاکتور محرک کُلونی گرانولوسیتTNF-α - فاکتور نکروز توموری آلفاmacrophage inflammatory protein-1 alpha - ماکروفاژ التهابی پروتئین 1 آلفاRANTES - مطالبHamilton Depression Rating Scale - مقیاس رتبه بندی افسردگی همیلتونselective serotonin reuptake inhibitors - مهار کننده های بازجذب سروتونین انتخابیEscitalopram - همزمان escitaloprammonocyte chemotactic protein 1 - پروتئین chemotactic monocyte 1interferon gamma-induced protein 10 - پروتئین ناشی از گاما اینترفرون 10Interferon gamma - گاما اینترفرون
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
علوم غدد
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
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.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Psychoneuroendocrinology - Volume 53, March 2015, Pages 246-255
Journal: Psychoneuroendocrinology - Volume 53, March 2015, Pages 246-255
نویسندگان
Pei-Shen Ho, Yi-Wei Yeh, San-Yuan Huang, Chih-Sung Liang,