Abstract # 1807 Systematic review of studies examining the effects of acute psychological stress on circulating inflammatory markers

• Published in: Brain, behavior, and immunity behavior, and immunity, 2016-10, Vol.57, p.e28-e28
• Main Authors: Lockwood, K.G, Walsh, C.P, John-Henderson, N.A, Marsland, A.L
• Format: Article
• Language: English
• Subjects: Allergy and Immunology; Psychiatry
• ISSN: 0889-1591; 1090-2139
• DOI: 10.1016/j.bbi.2016.07.095

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 before and after exposure to laboratory challenge. Results showed significant stress-related increases in interleukin(IL)-1 β ( d = 0.66, CI [0.21, 1.12], p < .001), IL-6 ( d = 0.31, CI [0.23, 0.39], p < .001), IL-10 ( d = 0.69, CI [0.03, 1.35], p < .001), and tumor necrosis factor(TNF)- α ( d = 0.28, CI [0.05, 0.51], p < .001), but not IL-1ra, IL-2, interferon-?, or C-reactive protein. There were sufficient data to assess the time course of IL-6 and TNF- α . For IL-6, there was a significant increase from baseline to post-stress measures at 40–50 min, 60–75 min, 90 min, and 120 min, with the largest effect at 90 min post-stress ( d = 0.70, CI [0.45, 0.95], p < .001). For TNF- α , there was a significant increase from baseline to post-stress measurement at 31–50 min ( d = 0.17, CI [0.10, 0.78], Z = 2.51, p = .01). There was no significant difference in magnitude of IL-6 reactivity as a function of type of stress (social-evaluative versus other). These results extend findings from a prior meta-analysis (Steptoe et al., 2007), showing reliable increases in IL-6, IL-1 β , IL-10 and TNF- α in response to acute stress. It is possible that these responses provide a pathway mediating relationships between exposure to life challenges and vulnerability to inflammatory disease.