The effects of acute psychological stress on circulating and stimulated inflammatory markers: A systematic review and meta-analysis
By Anna L. Marsland, Catherine P. Walsh, Kimberly G. Lockwood, Neha A. John-Henderson. Brain, behavior, and immunity, 2017
610 citations recorded by the source corpus.
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 < .001), IL-6 (d = 0.35, p < .001), IL-10 (d = 0.69, p < .001), and tumor necrosis factor(TNF)-α (d = 0.28, p < .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 120 min following stress, with the largest effect at 90min post-stress (d = 0.70, p < .001). IL-1β increased from baseline to 20–30, 40–50, and 60–70 min following stress, with the largest effect between 40–50 min post-stress (d = .73, p = .02). For TNF-α, there was a significant increase from baseline to 31–50 min post stress (d = 0.44, p = .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 20–120 min post-stress (d = 1.09, p < .001), and in IL-4 and interferon-γ when measured 0–10 min post stressor (d = −0.42, p < .001 and d = 0.47, p < .001). These results extend findings from a prior meta-analysis (Steptoe, Hamer, & Chida, 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.
Subfields: Behavioral Neuroscience, Health, Toxicology and Mutagenesis, Psychiatry and Mental health
View Paper: https://www.semanticscholar.org/paper/116e681a9d85de2e50cb0ee247b1594007a360c7
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Citations in the corpus
- More than a feeling: A unified view of stress measurement for population science (2018, background): “Inflammatory processes, which are consistently upregulated during periods of acute and prolonged stress (Marsland et al., 2017; Segerstrom and Miller, 2004) are also implicated in signaling the brain in ways relevant to the processing of stressors.”
- Rethinking IL-6 and CRP: Why they are more than inflammatory biomarkers, and why it matters. (2018, neutral): “The rise of IL-6 is slower and reaches a peak after 90-120 minutes (Marsland et al., 2017; Segerstrom & Miller 2004; Steptoe et al, 2007).”
- The Vagus Nerve at the Interface of the Microbiota-Gut-Brain Axis (2018, background): “A single acute stress induces a prolonged increase of pro-inflammatory cytokines after the end of stress exposition (Marsland et al., 2017), at the moment of the recovery period which is a critical period since it corresponds to the parasympathetic rebound.”