Marsland Anna L, Walsh Catherine, Lockwood Kimberly, John-Henderson Neha A
Department of Psychology, University of Pittsburgh, United States.
Department of Psychology, University of Pittsburgh, United States.
Brain Behav Immun. 2017 Aug;64:208-219. doi: 10.1016/j.bbi.2017.01.011. Epub 2017 Jan 12.
Inflammatory reactivity to acute laboratory stress is thought to reflect individual differences in responsivity to environmental stressors and may confer future health risk. To characterize this response, we conducted a meta-analysis of 34 studies that measured circulating inflammatory markers and 15 studies that measured stimulated production of inflammatory markers before and after exposure to laboratory challenge. Results showed significant stress-related increases in circulating interleukin (IL)-1β (d=0.66, p<0.001), IL-6 (d=0.35, p<0.001), IL-10 (d=0.69, p<0.001), and tumor necrosis factor(TNF)-α (d=0.28, p<0.001), but not IL-1ra, IL-2, interferon-γ, or C-reactive protein. There were sufficient data to assess the time course of IL-6, IL-1β, and TNF-α reactivity. IL-6 increased from baseline to measures taken 40-50, 60-75, 90, and 120min following stress, with the largest effect at 90min post-stress (d=0.70, p<0.001). IL-1β increased from baseline to 20-30, 40-50, and 60-70min following stress, with the largest effect between 40 and 50min post-stress (d=0.73, p=0.02). For TNF-α, there was a significant increase from baseline to 31-50min post stress (d=0.44, p=0.01), but not at later times. There was no difference in magnitude of IL-6 reactivity as a function of type of stress (social-evaluative versus other). For stimulated inflammatory markers, results showed stress-related increases in IL-1β when measured 20-120min post-stress (d=1.09, p<0.001), and in IL-4 and interferon-γ when measured 0-10min post stressor (d=-0.42, p<0.001 and d=0.47, p<0.001). These results extend findings from a prior meta-analysis (Steptoe et al., 2007) to show reliable increases in circulating IL-6, IL-1β, IL-10 and TNF-α and stimulated IL-1β, IL-4 and interferon-γ in response to acute stress. It is possible that these responses contribute to associations between exposure to life challenges and vulnerability to inflammatory disease.
对急性实验室应激的炎症反应被认为反映了个体对环境应激源反应性的差异，并可能带来未来的健康风险。为了描述这种反应，我们对34项测量循环炎症标志物的研究和15项测量暴露于实验室挑战前后炎症标志物刺激产生的研究进行了荟萃分析。结果显示，应激相关的循环白细胞介素（IL）-1β（d=0.66，p<0.001）、IL-6（d=0.35，p<0.001）、IL-10（d=0.69，p<0.001）和肿瘤坏死因子（TNF）-α（d=0.28，p<0.001）显著增加，但IL-1ra、IL-2、干扰素-γ或C反应蛋白没有增加。有足够的数据来评估IL-6、IL-1β和TNF-α反应性的时间进程。IL-6从基线增加到应激后40-50、60-75、90和120分钟时的测量值，在应激后90分钟时影响最大（d=0.70，p<0.001）。IL-1β从基线增加到应激后20-30、40-50和60-70分钟，在应激后40至50分钟之间影响最大（d=0.73，p=0.02）。对于TNF-α，从基线到应激后31-50分钟有显著增加（d=0.44，p=0.01），但在之后的时间没有增加。IL-6反应性的大小在应激类型（社会评价性与其他）方面没有差异。对于刺激的炎症标志物，结果显示应激后20-120分钟测量时IL-1β有应激相关的增加（d=1.09，p<0.001），应激源后0-10分钟测量时IL-4和干扰素-γ有增加（d=-0.42，p<0.001和d=0.47，p<0.001）。这些结果扩展了先前荟萃分析（Steptoe等人，2007年）的发现，表明急性应激反应时循环中的IL-6、IL-1β、IL-10和TNF-α以及刺激后的IL-1β、IL-4和干扰素-γ可靠增加。这些反应可能有助于解释生活挑战暴露与炎症性疾病易感性之间的关联。
