Kristin M Davis1, Christopher G Engeland2, Kyle W Murdock3. 1. Department of Biobehavioral Health, The Pennsylvania State University, United States. 2. Department of Biobehavioral Health, The Pennsylvania State University, United States; College of Nursing, The Pennsylvania State University, United States. 3. Department of Biobehavioral Health, The Pennsylvania State University, United States. Electronic address: kwm20@psu.edu.
Abstract
BACKGROUND: Empirical and theoretical evidence suggest that because of the co-evolution of the endocrine and immune response systems, different types of stressors may lead to similar levels of physiological activation. The present analyses examined associations between two physiological stress responses: the cortisol response to an acute laboratory stressor and ex vivo lipopolysaccharide (LPS) stimulated inflammatory cytokine production. METHODS: Healthy middle-aged adults (N = 65) completed testing at two appointments, two weeks apart. Blood was collected at each appointment to measure circulating inflammatory cytokine levels and stimulated inflammatory cytokine production after 4 and 24 hours of incubation with LPS. A cumulative standardized composite measure of inflammation was calculated using the cytokines interleukin-6 (IL-6), interleukin-1β (IL-1β), and interferon-γ (IFN-γ). At visit two, after the blood draw, participants completed the Trier Social Stress Test (TSST); saliva samples were collected before and after to generate cortisol response curves (area under the curve with respect to ground [AUCG] and increase/decrease [AUCI]). RESULTS: AUCG was significantly associated with stimulated cytokine production at visit 2 after both 4 hours (B = 6.89; p = 0.007) and 24 hours (B = 7.50; p = 0.005) of incubation, controlling for age, sex, and BMI. AUCI was also significantly associated with stimulated cytokine production at visit 2 after 4 hours (B = 6.28; p = 0.004) and 24 hours (B = 6.16; p = 0.007) of incubation, controlling for age, sex, and BMI. Stimulated inflammatory cytokine production was strongly correlated across the two visits (2 weeks apart) after 4 hours of incubation (r = 0.80, p < 0.001) and after 24 hours (r = 0.80, p < 0.001). Within each visit, stimulated cytokine production after 4 hours was significantly correlated with stimulated inflammation at 24 hours (r = 0.93-0.94, p < 0.05) CONCLUSIONS: These results suggest that LPS-stimulated inflammatory cytokine production and the cortisol response to the TSST contain comparable information about acute human physiological stress responses. Moreover, measurement of stimulated cytokines was highly stable across a two-week time period whether measured after 4 or 24 hours of incubation with LPS.
BACKGROUND: Empirical and theoretical evidence suggest that because of the co-evolution of the endocrine and immune response systems, different types of stressors may lead to similar levels of physiological activation. The present analyses examined associations between two physiological stress responses: the cortisol response to an acute laboratory stressor and ex vivo lipopolysaccharide (LPS) stimulated inflammatory cytokine production. METHODS: Healthy middle-aged adults (N = 65) completed testing at two appointments, two weeks apart. Blood was collected at each appointment to measure circulating inflammatory cytokine levels and stimulated inflammatory cytokine production after 4 and 24 hours of incubation with LPS. A cumulative standardized composite measure of inflammation was calculated using the cytokines interleukin-6 (IL-6), interleukin-1β (IL-1β), and interferon-γ (IFN-γ). At visit two, after the blood draw, participants completed the Trier Social Stress Test (TSST); saliva samples were collected before and after to generate cortisol response curves (area under the curve with respect to ground [AUCG] and increase/decrease [AUCI]). RESULTS: AUCG was significantly associated with stimulated cytokine production at visit 2 after both 4 hours (B = 6.89; p = 0.007) and 24 hours (B = 7.50; p = 0.005) of incubation, controlling for age, sex, and BMI. AUCI was also significantly associated with stimulated cytokine production at visit 2 after 4 hours (B = 6.28; p = 0.004) and 24 hours (B = 6.16; p = 0.007) of incubation, controlling for age, sex, and BMI. Stimulated inflammatory cytokine production was strongly correlated across the two visits (2 weeks apart) after 4 hours of incubation (r = 0.80, p < 0.001) and after 24 hours (r = 0.80, p < 0.001). Within each visit, stimulated cytokine production after 4 hours was significantly correlated with stimulated inflammation at 24 hours (r = 0.93-0.94, p < 0.05) CONCLUSIONS: These results suggest that LPS-stimulated inflammatory cytokine production and the cortisol response to the TSST contain comparable information about acute human physiological stress responses. Moreover, measurement of stimulated cytokines was highly stable across a two-week time period whether measured after 4 or 24 hours of incubation with LPS.
Authors: Erik L Knight; Marzieh Majd; Jennifer E Graham-Engeland; Joshua M Smyth; Martin J Sliwinski; Christopher G Engeland Journal: Physiol Behav Date: 2021-11-25
Authors: Karina Van Bogart; Christopher G Engeland; Martin J Sliwinski; Karra D Harrington; Erik L Knight; Ruixue Zhaoyang; Stacey B Scott; Jennifer E Graham-Engeland Journal: Front Behav Neurosci Date: 2022-01-11 Impact factor: 3.558