The effects of acute psychological stress on circulating and stimulated inflammatory markers: A systematic review and meta-analysis.
Level 1 - systematic review of randomized trials
Systematic review and meta-analysis of experimental laboratory challenge studies
PubMed 28089638 · doi:10.1016/j.bbi.2017.01.011
What was done
A systematic review and meta-analysis was conducted across 34 studies measuring circulating inflammatory markers and 15 studies measuring stimulated inflammatory marker production before and after exposure to acute laboratory psychological stress. Post-stress time courses were analyzed for IL-6, IL-1β, and TNF-α, and stressor type (social-evaluative versus other) was tested as a moderator of IL-6 reactivity.
What was found
Acute stress led to significant overall increases in circulating 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 TNF-α (d = 0.28, p < 0.001), but not IL-1ra, IL-2, interferon-γ, or C-reactive protein. Time-course analysis showed: - Circulating IL-6 increased at 40-50, 60-75, 90, and 120 min post-stress, peaking at 90 min (d = 0.70, p < 0.001). - Circulating IL-1β increased at 20-30, 40-50, and 60-70 min post-stress, peaking at 40-50 min (d = 0.73, p = 0.02). - Circulating TNF-α increased at 31-50 min post-stress (d = 0.44, p = 0.01), but not later. - Stressor type (social-evaluative vs. other) did not alter IL-6 reactivity magnitude. For stimulated markers, stress produced changes in stimulated IL-1β measured 20-120 min post-stress (d = 1.09, p < 0.001), stimulated IL-4 measured 0-10 min post-stress (d = -0.42, p < 0.001), and stimulated interferon-γ measured 0-10 min post-stress (d = 0.47, p < 0.001).
Why it matters
This review establishes the temporal dynamics and specific cytokine profile of human inflammatory reactivity to acute psychological challenge, identifying when circulating and stimulated immune markers peak after exposure.
Limits
The abstract does not report the total human participant sample size, demographics, or health status across studies. Laboratory stress paradigms may not fully generalize to naturalistic chronic or acute real-world stressors, and several inflammatory markers lacked sufficient data for time-course modeling.
Cited by
- supports Psychological stress causes physical inflammation in the body.