Lower inflammatory markers in women with antenatal depression brings the M1/M2 balance into focus from a new direction

Lower inflammatory markers in women with antenatal depression brings the M1/M2 balance into focus from a new direction
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DOI:
10.1016/j.psyneuen.2017.02.027
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发表时间:
2017-06-01
影响因子:
3.7
通讯作者:
Sundstrom-Poromaa, Inger
Sundstrom-Poromaa, Inger
中科院分区:
医学2区
文献类型:
--
作者:
Edvinsson, Asa;Brann, Emma;Sundstrom-Poromaa, Inger

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背景资料:妊娠期抑郁和使用5-羟色胺再摄取抑制剂(SSRI)都与不良妊娠结局的风险增加有关,如早产和胎儿生长受损。虽然对这些并发症的潜在生物学途径知之甚少,但已假设炎症可能是常见的生理学途径。本研究的目的是评估外周炎症标志物在健康妇女,妇女与产前抑郁症,并在妇女使用SSRI在pregnancy.Methods:160健康孕妇对照组,59名妇女与产前抑郁症和39名妇女与SSRIs治疗。92个炎症蛋白的相对水平进行了分析,通过邻近延伸检测technology.Results:总体而言,23个炎症标志物显着降低与健康对照组相比,产前抑郁症的妇女和妇女在治疗与SSRIs。在患有产前抑郁症的妇女和使用SSRI的妇女之间没有观察到任何炎症标志物的差异。在产前抑郁症妇女中下调的前三个炎症标志物是TNF相关凋亡诱导配体(TRAIL),p = 0.000001,巨噬细胞集落刺激因子1(CSF-1),p = 0.000004,和fractalkine(CX 3CL 1),p = 0.00005。SSRI使用者中相应的炎症标志物为CSF-1,p = 0.000011,血管内皮生长因子A(VEGF-A),p =0.000016和IL-15受体亚单位α(IL-15 RA),p = 0.000027。对照组的炎症标志物与可的松血清浓度呈负相关,而病例组则不相关。在一个独立的表观遗传学coherent.Conclusion:产前抑郁症或SSRI治疗的妇女有较低水平的一些外周炎症标志物比健康的孕妇对照组,这些炎症标志物的差异DNA甲基化。假设,这可能是由于正常晚期妊娠特征的前M2环境的失调转换。然而,纵向血液采样是必要的,以阐明是否可能失调的M2移位是驱动产前抑郁症的发展,或抑郁症的结果。(C)2017爱思唯尔有限公司版权所有
Background: Antenatal depression and use of serotonin reuptake inhibitors (SSRI) in pregnancy have both been associated with an increased risk of poor pregnancy outcomes, such as preterm birth and impaired fetal growth. While the underlying biological pathways for these complications are poorly understood, it has been hypothesized that inflammation may be a common physiological pathway. The aim of the present study was to assess peripheral inflammatory markers in healthy women, women with antenatal depression, and in women using SSRI during pregnancy.Methods: 160 healthy pregnant controls, 59 women with antenatal depression and 39 women on treatment with SSRIs were included. The relative levels of 92 inflammatory proteins were analyzed by proximity extension assay technology.Results: Overall, 23 of the inflammatory markers were significantly lower in women with antenatal depression and in women on treatment with SSRIs in comparison with the healthy controls. No difference in any of the inflammatory markers was observed between women with antenatal depression and those who were using SSRI. Top three inflammatory markers that were down-regulated in women with antenatal depression were TNF-related apoptosis-inducing ligand (TRAIL), p = 0.000001, macrophage colony-stimulating factor 1 (CSF-1), p = 0.000004, and fractalkine (CX3CL1), p =0.000005. Corresponding inflammatory markers in SSRI users were CSF-1, p = 0.000011, vascular endothelial growth factor A (VEGF-A), p =0.000016, and IL-15 receptor subunit alpha (IL-15RA), p = 0.000027. The inflammatory markers were negatively correlated with cortisone serum concentrations in controls, but not in the cases. Differential DNA methylation of was found for seven of these inflammatory markers in an independent epigenetics cohort.Conclusion: Women with antenatal depression or on SSRI treatment have lower levels of a number of peripheral inflammatory markers than healthy pregnant controls. Hypothetically, this could be due to dysregulated switch to the pro-M2 milieu that characterizes normal third trimester pregnancy. However, longitudinal blood sampling is needed to elucidate whether the presumably dysregulated M2 shift is driving the development of antenatal depression or is a result of the depression. (C) 2017 Elsevier Ltd. All rights reserved.