Acute mental stress elicits delayed increases in circulating inflammatory cytokine levels

Abstract

The influence of acute mental stress on cardiovascular responses and concentrations of inflammatory cytokines up to 2 h later was assessed in 12 subjects exposed to stress and in eight control subjects. Beat-by-beat recordings of finger blood pressure and heart rate were made at rest and during two behavioural tasks (colour-word interference and mirror tracing). Blood was drawn after adaptation and at 45 min and 2 h after the tasks, and assayed for interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α), interleukin-1 receptor antagonist (IL-1Ra), C-reactive protein (CRP) and haematocrit. Saliva was sampled periodically and assayed for free cortisol. The tasks were rated as stressful by the participants. The stress group showed significant increases in systolic and diastolic blood pressure (mean rises of 16.4p12.3 and 12.6p6.9 mmHg respectively) and heart rate (5.39p5.3 beats/min) ; these values returned to baseline during the recovery period. The IL-6 concentration was increased by 56 % at 2 h after the tasks (P 0.05), while IL1Ra was increased by 12.3 % (P 0.01). No changes in cardiovascular variables or cytokine concentrations were observed in the control subjects, and haematocrit did not change. The magnitude of blood pressure responses during tasks was correlated positively with the IL-6 concentration after 45 min (r l 0.70, P 0.05), and with the IL-1Ra concentration after 2 h (r l 0.63, P 0.05). Increases in TNF-α after 2 h were correlated with heart rate responses to tasks (r l 0.66, P 0.05). Associations between IL-6 and IL-1Ra concentrations were also recorded. This study indicates that inflammatory cytokines respond to acute mental stress in humans with delayed increases, and suggest that individual differences in cytokine responses are associated with sympathetic reactivity.

A mechanism converting psychosocial stress into mononuclear cell activation

“…Further downstream signals converting psychosocial stress into cellular dysfunction and finally into vascular disease are still largely unknown. One observation pointing to a potential mechanism is the induction of inflammatory reactions and the simultaneous decrease of antiinflammatory reactions leading to enhanced cytokine release and monocytic cell activation (19)(20)(21)(22)(23). These changes in mononuclear properties are consistent with the activation of the redox-sensitive transcription factor nuclear factor B (NF-B) (24)(25)(26)(27)(28)(29).…”

Cardiovascular stress responsivity, body mass and abdominal adiposity

“…We have previously observed that acute increases in plasma interleukin 6 (IL-6) and tumour necrosis factor (TNF) a are stimulated by psychological stress. 41,42 Heightened IL-6 levels may contribute to the development of abdominal adiposity. Much of the IL-6 produced through sympathetic activation originates from adipose tissue, 43 and in turn stimulate HPA pathways contributing to abdominal adiposity.…”

Stress-induced release of matrix metalloproteinase-9 in patients with coronary artery disease: The possible influence of cortisol

“…According to previous studies, a peak response in cortisol is expected to occur 15-25 min after a laboratory mental stressor followed by a rapid decline reaching below pre-test levels (Kunz-Ebrecht et al 2003, Brydon 2010, McInnis et al 2015. However, in one study of healthy volunteers, cortisol levels were shown to be lower already 20 min after stress compared with pre-test levels (Steptoe et al 2001). Interestingly, Kunz-Ebrecht et al (Kunz-Ebrecht et al 2003) reported that cortisol levels 20 min after stress were lower than pre-test levels in those individuals who exhibited the lowest cortisol response to stress, so-called cortisol non-responders.…”