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Cited by 691Stress Responses and CortisolTryptophan and brain disordersCancer, Stress, Anesthesia, and Immune Response

The effects of acute psychological stress on circulating and stimulated inflammatory markers: a systematic review and meta-analysis

Open access
Marsland, Anna L., Walsh, Catherine, Lockwood, Kimberly, John-Henderson, Neha A.·2017·Brain, Behavior, and Immunity
DOI 10.1016/j.bbi.2017.01.011PMC PMC5553449
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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)-1β (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)-α (d=0.28, p<0.001), 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 120min following stress, with the largest effect at 90min post-stress (d=0.70, p<0.001). IL-1β increased from baseline to 20-30, 40-50, and 60-70min following stress, with the largest effect between 40 and 50min post-stress (d=0.73, p=0.02). For TNF-α, there was a significant increase from baseline to 31-50min 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-1β when measured 20-120min post-stress (d=1.09, p<0.001), and in IL-4 and interferon-γ when measured 0-10min 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-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.

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Crossref · 10.1016/j.bbi.2017.01.011

Cites

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  • Inflammatory processes are consistently upregulated during periods of acute and prolonged stress.

    “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.”

    From More than a feeling: A unified view of stress measurement for population science (2018) · cites this paper as Marsland et al., 2017

    The Discussion’s “Mechanisms of change” section reports increased pro-inflammatory cytokines after brief laboratory stress. The “Limitations and Future Directions” section says it remains uncertain whether those findings generalize to naturally occurring stressors. The paper therefore supports upregulation with acute laboratory stress, but not the claim that it consistently occurs during prolonged stress. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Acute psychological stress elevates circulating levels of inflammatory markers such as CRP and IL-6.

    “In thorough reviews, Steptoe et al. (2007) and Marsland et al. (2017) showed that acute psychological stress leads to the elevation of the circulating levels of inflammatory markers such as C-reactive protein (CRP) and interleukin-6 (IL-6).”

    From Strong Enough to Suffer: Emotional Suppression, Stress Exposure, and Physiological Health Among Men Across the Life Course (2026) · cites this paper as Marsland et al., 2017

    The Results (Circulating Inflammatory Markers) report increased circulating IL-6 from 11–120 minutes after acute stress. The same section finds no significant change in circulating CRP, so the claim is supported for IL-6 but not CRP. (LLM, conf=0.93)

    Experimental — accuracy not yet measured

  • Both acute and chronic psychosocial stressors in humans have been reliably associated with systemic inflammatory responses.

    “Indeed, both acute and chronic psychosocial stressors in humans have been reliably associated with systemic inflammatory responses [15,16].”

    From Immune Cell Ratios Are Higher in Bipolar Affective than Unipolar Depressive Disorder and Modulated by Mood Episode: A Retrospective, Cross-Sectional Study (2023) · cites this paper as [16]

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Research works printed but not linked: 2

  1. Borenstein M Hedges LV Higgins JPT Rothstein HR 2009 Introduction to Meta-Analnsts John Wiley & Sons Ltd, Chichester, UK
  2. Moher D Liberati A Tetzlaff J Altman DG 2009 PRISMA Group J Clin Epidemiol 62 10 1006 12 19631508

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Authors
Marsland, A. L., Walsh, C., Lockwood, K., & John-Henderson, N. A.
Affiliations
University of Pittsburgh (US)
Corresponding author
Marsland, Anna L.
ORCID
Venue
Brain, Behavior, and Immunity
Publisher
Elsevier BV
Published
2017-08
Volume
64
Pages
208-219
ISSN
0889-1591 (ISSN-L)
DOI
10.1016/j.bbi.2017.01.011
PMC
PMC5553449
OpenAlex
W2576595026
Cited by
691
References
117
Citations by year
2026: 72 · 2025: 95 · 2024: 70 · 2023: 74 · 2022: 90 · 2021: 85 · 2020: 87 · 2019: 54 · 2018: 46 · 2017: 16
FWCI
4.91
Type
journal article
Language
en
Open access
Licence
Locations
  • Brain Behavior and Immunity (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institute of Health
Topics
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Health Sciences › Medicine › Psychiatry and Mental health › Cancer, Stress, Anesthesia, and Immune Response
Keywords
acute psychological stress, inflammatory markers, interleukin-6, IL-1β, TNF-α, IL-10, IL-4, interferon-gamma, laboratory stress, social-evaluative stress, health risks, cytokines, C-reactive protein, interleukin-1 receptor antagonist, interleukin-2, IL-12/23
MeSH terms
Humans, Inflammation, Stress, Psychological, Biomarkers, Inflammation Mediators

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