Short sleep duration in the natural environment may negatively affect in vivo antibody responses to novel antigens, providing a possible explanation for observed associations of poor sleep with increased susceptibility to infectious disease.
Laboratory studies show that individuals differ appreciably in the magnitude of their inflammatory responses to acute psychological stress. These individual differences are poorly understood, yet may contribute to variation in stress-associated disease vulnerability. The present study examined the possibility that affective responses to acute stress contribute to these differences. For this purpose, 102 relatively-healthy community volunteers (mean age 50 years; 60% female; 91.2% white) performed an acute stress protocol and measures of affective state and serum levels of the proinflammatory cytokine, interleukin (IL)-6 were collected at the end of a 30-min resting baseline, a 5-min evaluative public speaking task, and a 30-min recovery period. Results of regression analyses, controlling for age, race, gender, menopausal status, and body mass index, revealed a positive association of task-related increases in anger and anxiety with increases in IL-6 (R 2 change = .08, p = .004; R 2 change = .08, p = .005, respectively). Further examination showed that these affective responses to the task were independent predictors of change in IL-6. Cardiovascular reactivity to the task did not explain the association. These results suggest that individuals who exhibit angry or anxious responses to acute challenge are more vulnerable to stress-related increases in markers of systemic inflammation, possibly rendering them more susceptible to inflammatory disease.
Emerging evidence suggests that acute psychological stress modulates inflammatory competence; however, not all findings are consistent. Gender is one factor that may impact magnitude of response. To explore this possibility, we examined the effects of acute mental stress on lipopolysaccharideinduced production of pro-inflammatory cytokines interleukin (IL)-1 β, IL-6, and tumor necrosis factor (TNF)-α among a relatively healthy sample of midlife men (n=28) and women (n=34). Blood samples for the assessment of cytokine production were drawn before, immediately after and 30 minutes following subjects' performance of an evaluative speech task. Relative to baseline evaluations, the speech stressor elicited a significant increase in stimulated production of all 3 proinflammatory cytokines, as measured 30 minutes following the end of the task. There were no gender differences in the magnitude of this effect. However, men showed a significant decrease in cytokine production from before to immediately following the stressor, whereas women showed no change across this period. Menopausal status partially accounted for these gender differences, with postmenopausal women displaying greater increases in IL-6 and TNF-α production from baselineto-post task when compared to men. These data provide further evidence that acute psychological stress primes the immune system to mount larger inflammatory responses and initial support for gender differences in the patterning of stress-related cytokine activity. In addition, this study presents novel evidence that post-menopausal women may be particularly susceptible to stress-related inflammatory responses. The possibility that this contributes to the increased risk of inflammatory disease observed among older women warrants investigation.
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