Variations in anticipatory cognitive stress appraisal and differential proinflammatory cytokine expression in response to acute stress

Abstract

Objective Anticipatory cognitive appraisal can affect the stress-induced release of stress hormones and stress hormones can modulate monocyte cytokine expression. We investigated whether anticipatory cognitive appraisal processes would predict changes in monocyte cytokine expression following psychosocial stress in relation to stress hormone release. Methods Forty-four men (mean age 43 ± 2 years; mean arterial blood pressure (MAP) 102 ± 2 mm Hg; mean body mass index (BMI) 26 ± .4 kg/m 2) completed the Primary Appraisal Secondary Appraisal (PASA) scale before undergoing the Trier Social Stress Test (combination of mock job interview and mental arithmetic task). Lipopolysaccharide (LPS)-stimulated tumor necrosis factor (TNF)-α and interleukin (IL)-6 expression by monocytes was assessed in vitro immediately before and after stress, and during recovery up to 60 min post-stress. Moreover, we repeatedly measured salivary cortisol as well as plasma epinephrine and norepinephrine levels. Results Stress hormones increased and cytokines decreased following stress (all p < 0.05). Correlation analyses showed that a higher PASA “stress index” was associated with higher expression (area under the curve, AUC) of total LPS-stimulated TNF-α ( r = .33, p = .03) and IL-6 ( r = .32, p = .33) between rest and 60 min post-stress. While controlling for age, BMI, and MAP, higher values in the primary PASA scale “control expectancy” predicted lower TNF-α expression following stress ( ß = −.42, p = 0.003). Higher “control expectancy” ( ß = −.32, p = 0.031) and lower “challenge” ( ß = .30, p = 0.046) predicted lower IL-6 expression. None of the stress hormones predicted expression of any cytokine. Conclusions We found that anticipatory cognitive stress appraisal modulates monocyte inflammatory activity following stress suggesting that interventions aiming at improving coping skills might modify the monocyte cytokine response.