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 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 α (d = 0.28, CI [0.05, 0.51], p 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 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.

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