Article
The effects of acute psychological stress on circulating and stimulated inflammatory markers: A systematic review and meta-analysis
Authors
Anna L. Marsland, Catherine Walsh, Kimberly Lockwood, Neha A. John-Henderson
Publication
Brain, Behavior, and Immunity
Abstract
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)-1? (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)-? (d = 0.28, p < 0.001), but not IL-1ra, IL-2, interferon-?, or C-reactive protein. There were sufficient data to assess the time course of IL-6, IL-1?, and TNF-? reactivity. IL-6 increased from baseline to measures taken 40–50, 60–75, 90, and 120 min following stress, with the largest effect at 90 min post-stress (d = 0.70, p < 0.001). IL-1? increased from baseline to 20–30, 40–50, and 60–70 min following stress, with the largest effect between 40 and 50 min post-stress (d = 0.73, p = 0.02). For TNF-?, there was a significant increase from baseline to 31–50 min 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-1? when measured 20–120 min post-stress (d = 1.09, p < 0.001), and in IL-4 and interferon-? when measured 0–10 min 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-1?, IL-10 and TNF-? and stimulated IL-1?, IL-4 and interferon-? in response to acute stress. It is possible that these responses contribute to associations between exposure to life challenges and vulnerability to inflammatory disease.
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