Depressive symptoms post hip fracture in older adults are associated with phenotypic and functional alterations in T cells.

Depressive symptoms post hip fracture in older adults are associated with phenotypic and functional alterations in T cells.
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DOI:
10.1186/s12979-014-0025-5
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发表时间:
2014
期刊:
Immunity & ageing : I & A
影响因子:
--
通讯作者:
Lord JM
Lord JM
中科院分区:
其他
文献类型:
--
作者:
Duggal NA;Upton J;Phillips AC;Hampson P;Lord JM

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衰老伴随着免疫力下降,称为免疫衰老。免疫系统不是孤立地起作用的,它对心理和生理压力都很敏感。髋部骨折是老年人常见的生理应激源,新发抑郁症发生率高,预后差。因此,我们开始研究身体压力(髋部骨折)和心理压力(抑郁症状)对老年人免疫系统可能产生的协同效应。对101名髋部骨折患者(81名女性)和43名年龄匹配的健康对照组(26名女性)在髋部骨折后6周的T细胞表型和功能进行了评估。38例骨折患者6周时出现抑郁症状。与健康对照组相比,抑郁症髋部骨折患者的T细胞频率(p = 0.01)和数量(p = 0.003)均较低。衰老CD28-ve的频率(p =。001), CD57+ve (p =。001), KLRG1+ve (p =。03) CD8 T细胞,以及衰老的CD28-ve CD4+ve (p = 0.01)和CD57+ve CD4+ve (p = 0.01)。(3)抑郁症髋部骨折患者的T细胞比健康对照组高,CD28-ve CD8 T细胞的频率也比单纯髋部骨折患者高(p = 0.01)。此外,活化CD69+ve (p = 0.005)和HLADR+ve (p < 0.05)。与健康对照组相比,抑郁症髋部骨折患者的CD8 T细胞含量也更高。通过活化T细胞检测细胞因子的产生,与健康对照相比,在伴有抑郁症状的髋部骨折患者的CD4 T细胞中观察到TNFα (p = 0.03)和IL6 (p = 0.04)的产生显著增加。由于研究中没有患者有抑郁症病史,我们的数据表明,髋部骨折患者抑郁症状的发展与T细胞表型改变和促炎功能增加有关,而这在髋部骨折后未发生抑郁的患者中未见。因此,及时治疗髋部骨折患者的抑郁症状可能会改善这些患者的免疫力和预后。本文的在线版本(doi:10.1186/s12979-014-0025-5)包含补充材料,可供授权用户使用。
Ageing is accompanied by reduced immunity, termed immunesenescence. The immune system does not act in isolation and is sensitive to both psychological and physical stress. Hip fracture is a common physical stressor in older adults with a high incidence of new onset depression, which relates to poorer prognosis. We therefore set out to examine the possible synergistic effects of physical stress (hip fracture) and psychological stress (depressive symptoms) on the aged immune system. T cell phenotype and function was assessed in 101 hip fracture patients (81 female) 6 weeks after hip fracture and 43 healthy age-matched controls (26 female). 38 fracture patients had depressive symptoms at 6 weeks. T cell frequency (p = .01) and numbers (p = .003) were both lower in depressed hip fracture patients compared to healthy controls. The frequency of senescent CD28-ve (p = .001), CD57+ve (p = .001), KLRG1+ve (p = .03) CD8 T cells, as well as senescent CD28-ve CD4+ve (p = .01) and CD57+ve CD4+ve (p = .003) T cells were higher in depressed hip fracture patients compared with healthy controls and the frequency of CD28-ve CD8 T cells was also higher when compared to patients with hip fracture alone (p = .01). Additionally, activated CD69+ve (p = .005) and HLADR+ve (p < .001) CD8 T cells, were also higher in depressed hip fracture patients compared to healthy controls. On examining cytokine production by activated T cells, a significant increase in TNFα (p = .03) and IL6 (p = .04) production was observed in CD4 T cells from hip fracture patients with depressive symptoms compared to healthy controls. As none of the patients in the study had a prior history of depression, our data suggest that the development of depressive symptoms in hip fracture patients is associated with altered T cell phenotype and increased pro-inflammatory function which is not seen in patients who do not develop depression after hip fracture. Treating depressive symptoms promptly in hip fracture patients may therefore improve immunity and outcomes in these patients. The online version of this article (doi:10.1186/s12979-014-0025-5) contains supplementary material, which is available to authorized users.
人类天真,中央记忆和效应记忆CD4(+)T细胞的细胞因子驱动的增殖和分化。
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