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

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 < .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.

Posttraumatic stress disorder is associated with enhanced interleukin-6 response to mental stress in subjects with a recent myocardial infarction

“…We hypothesized that subjects with MI and PTSD would show an increased inflammatory response to acute psychological stress compared with those without PTSD. Specifically, we hypothesized that acute stress would be associated with a greater increase in IL-6 in MI patients with PTSD, as this inflammatory marker is known to be responsive to acute stress (Marsland et al, 2017). Our study also examined other established inflammatory biomarkers associated with CHD progression and/or PTSD, including ICAM-1, VCAM-1, high sensitivity C-reactive protein (HsCRP), matrix metallopeptidase-9 (MMP-9), and monocyte chemoattractant protein (MCP)-1 (Blankenberg et al; Blankenberg et al, 2003; de Lemos et al; Fanola et al; Held et al; Ridker; Sumner et al, 2017; Zakynthinos and Pappa), given that their relationship with acute stress and with PTSD has not been fully studied in patients with CHD.…”

Are Inflammatory Cytokines Associated with Pain during Acute Myocardial Infarction?

“…Both acute and chronic psychosocial stress have been associated with the release of proinflammatory cytokines, e.g., TNF-α and IL-6 [12][13][14][15] , and, as mentioned above, pain and acute psychological distress are correlated during AMI.…”

Cytokines as inducers of postperfusion systemic inflammatory reaction in cardiosurgical patients with different duration of coronary pathology

“…К одним из центральных медиаторов стрес-са относится IL-6 [14], который у пациентов с быстро прогрессирующей ИБС становится веду-щим провоспалительным цитокином в патогенезе послеоперационной СВР (см. табл.…”