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针对急性实验室应激源的免疫细胞动力学:早年逆境对生物学影响的个体内组间分析。

Immune cell dynamics in response to an acute laboratory stressor: a within-person between-group analysis of the biological impact of early life adversity.

机构信息

Department of Biobehavioral Health, The Pennsylvania State University, University Park, PA, USA.

Department of Psychology and Department of Communication, Stanford University, Stanford, CA, USA.

出版信息

Stress. 2022 Jan;25(1):347-356. doi: 10.1080/10253890.2022.2148100.

DOI:10.1080/10253890.2022.2148100
PMID:36404775
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9704543/
Abstract

Early life adversity (ELA) is a risk factor for early onset morbidities and mortality, a relationship that may be driven in part by immune system dysregulation. One mechanism of dysregulation that has yet to be fully examined in the context of ELA is alterations to immune cell dynamics in response to acute stress. Using a within-person between-group experimental design, we investigated stress-induced changes in immune cell populations, and how these changes may be altered in individuals with a history of ELA. Participants were young adults ( = 34, aged 18-25 years, 53% female, 47% with a history of ELA). Complete immune cell counts were measured at four time-points over a 5-hour window across two sessions (Trier Social Stress Test [TSST] vs. no-stress) separated by a week. Across all participants, total white blood cells increased over time ((3,84)=38.97,  < .001) with a greater increase in response to the TSST compared to the no-stress condition at 240 minutes post-test ( = 0.43±.19; (179)=2.22,  = .027). This pattern was mirrored by neutrophil counts. Lymphocyte counts were initially depressed by TSST exposure ( =-205±.67; (184)=-3.07,  = .002) but recovered above baseline. ELA status was associated with higher stress-induced immune cell counts, a difference likely driven by increases in neutrophils ((1,22)=4.45,  = .046). Overall, these results indicate differential immune cell dynamics in response to acute stress in individuals with a history of ELA. This points to altered immune system functioning in the context of stress, a finding that may be driving increased morbidity and mortality risk for ELA-exposed individuals.

摘要

早期生活逆境(ELA)是早发性发病和死亡的风险因素,这种关系部分可能是由免疫系统失调驱动的。在 ELA 背景下,尚未完全研究的失调机制之一是免疫细胞对急性应激的反应动态变化。我们采用个体内组间实验设计,研究了应激诱导的免疫细胞群体变化,以及这些变化在经历 ELA 的个体中如何改变。参与者为年轻成年人( = 34 名,年龄 18-25 岁,53%为女性,47%有 ELA 病史)。在两个会话(特里尔社会应激测试[TSST]与无应激)之间隔一周的 5 小时窗口内,在四个时间点测量完整的免疫细胞计数。在所有参与者中,总白细胞数随时间增加((3,84)=38.97, < .001),与无应激条件相比,在测试后 240 分钟对 TSST 的反应增加更大( = 0.43±.19;(179)=2.22,  = .027)。这种模式与中性粒细胞计数相吻合。淋巴细胞计数最初因 TSST 暴露而降低( =-205±.67;(184)=-3.07,  = .002),但恢复到基线以上。ELA 状态与应激诱导的免疫细胞计数增加有关,这种差异可能是由中性粒细胞增加引起的((1,22)=4.45,  = .046)。总的来说,这些结果表明,有 ELA 病史的个体对急性应激的免疫细胞反应存在差异。这表明在应激背景下免疫系统功能发生改变,这一发现可能是 ELA 暴露个体发病率和死亡率增加的原因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7866/9704543/bd8b33fffed6/nihms-1852122-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7866/9704543/84f6998aebb5/nihms-1852122-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7866/9704543/7a6fefe23af7/nihms-1852122-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7866/9704543/bd8b33fffed6/nihms-1852122-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7866/9704543/84f6998aebb5/nihms-1852122-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7866/9704543/7a6fefe23af7/nihms-1852122-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7866/9704543/bd8b33fffed6/nihms-1852122-f0003.jpg

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