Linsley Victoria G, Bishop Nicolette C, Roberts Matthew J, Hamrouni Malik, Demashkieh Mayada, Paine Nicola J
From the School of Sport, Exercise and Health Sciences, National Centre for Sport and Exercise Medicine, Loughborough University (Linsley, Bishop, Roberts, Hamrouni, Demashkieh, Paine), Loughborough; and National Institute for Health Research (NIHR) Leicester Biomedical Research Centre, University Hospitals of Leicester NHS Trust and the University of Leicester (Bishop, Roberts, Paine), Leicester, United Kingdom.
Biopsychosoc Sci Med. 2025;87(2):107-117. doi: 10.1097/PSY.0000000000001367.
Acute psychological stress is a risk factor for cardiovascular disease (CVD), possibly through promoting a heightened inflammatory profile. Active stressors are commonly used to investigate cardiovascular and immune reactivity; however, this response may not translate to other stress modalities. We aimed to decipher potential differences in immune responses to passive and active stressors.
Eighty-eight participants completed this study. After a baseline period, a passive (International Affective Picture System [IAPS]) and active stress task (Paced Auditory Serial Addition Test [PASAT]) were completed in a randomized order, with 45-minute rest post-tasks. Cardiovascular measures (including SBP, DBP, HR) were collected continuously. Blood samples were collected after each time point determining inflammatory responses, including circulating and stimulated interleukin-6 (IL-6), systemic inflammation response index (SIRI), neutrophil/lymphocyte ratio (NLR), TNF-α, and P- and E-selectin.
Cardiovascular measures were higher during the PASAT than IAPS (p < .001). Circulating IL-6 levels increased from baseline to 45-minutes after both tasks (p ≤ .001), with no difference between 45-minute post-PASAT and 45-minute post-IAPS (p > .05). SIRI increased from baseline to post-IAPS (p = .013), 45-minute post-IAPS (p = .004), and 45-minute post-PASAT (p < .001). No difference in SIRI between 45-minute post-PASAT and 45-minute post-IAPS existed. NLR increased from baseline to 45-minute post-PASAT (p = .008). There were no significant time effects for TNF-α, P-selectin, or E-selectin (all p > .05).
Both stressors increased circulating IL-6 levels and SIRI. Cardiovascular measures were higher during the active task, but the magnitude of inflammatory responses did not significantly differ between tasks. Regardless of stress modality, an immune response ensues, potentially increasing the risk of CVD over time.
急性心理应激是心血管疾病（CVD）的一个危险因素，可能是通过促进炎症反应增强来实现的。主动应激源常用于研究心血管和免疫反应；然而，这种反应可能不适用于其他应激方式。我们旨在解读对被动和主动应激源的免疫反应中的潜在差异。
88名参与者完成了本研究。在基线期之后，以随机顺序完成一项被动（国际情感图片系统[IAPS]）和一项主动应激任务（听觉连续加法测试[PASAT]），任务后休息45分钟。连续收集心血管指标（包括收缩压、舒张压、心率）。在每个确定炎症反应的时间点后采集血样，包括循环和刺激后的白细胞介素-6（IL-6）、全身炎症反应指数（SIRI）、中性粒细胞/淋巴细胞比值（NLR）、肿瘤坏死因子-α以及P-选择素和E-选择素。
PASAT期间的心血管指标高于IAPS（p <.001）。两项任务后循环IL-6水平均从基线升至45分钟时（p≤.001），PASAT后45分钟与IAPS后45分钟之间无差异（p>.05）。SIRI从基线升至IAPS后（p =.013）、IAPS后45分钟（p =.004）以及PASAT后45分钟（p <.001）。PASAT后45分钟与IAPS后45分钟之间的SIRI无差异。NLR从基线升至PASAT后45分钟（p =.008）。肿瘤坏死因子-α、P-选择素或E-选择素无显著的时间效应（所有p>.05）。
两种应激源均增加了循环IL-6水平和SIRI。主动任务期间的心血管指标更高，但任务之间的炎症反应程度无显著差异。无论应激方式如何，都会随之产生免疫反应，随着时间推移可能增加患CVD的风险。
