Negative affective responses to a speech task predict changes in interleukin (IL)-6.

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 (R² change = .08, p = .004; R² 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.

Gender differences in stimulated cytokine production following acute psychological stress.

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 lipopolysaccharide-induced production of pro-inflammatory cytokines interleukin (IL)-1beta, IL-6, and tumor necrosis factor (TNF)-alpha 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 30min 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 pro-inflammatory cytokines, as measured 30min 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 post-menopausal women displaying greater increases in IL-6 and TNF-alpha production from baseline-to-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.

Sleep and antibody response to hepatitis B vaccination.

STUDY OBJECTIVES: Experimental evidence links poor sleep with susceptibility to infectious illness; however, it remains to be determined if naturally occurring sleep is associated with immune responses known to play a role in protection against infection. The aim of this study was to determine whether sleep duration, sleep efficiency, and sleep quality, assessed in the natural environment, predict magnitude of antibody responses to a novel antigen among community volunteers in midlife. DESIGN: Observational. MEASUREMENTS AND RESULTS: Healthy midlife adults (n = 125; 70 female; age 40-60 yr) received the standard 3-dose hepatitis B vaccination series. Actigraphy and electronic sleep diaries were used to assess sleep duration, sleep efficiency, and subjective sleep quality. Viral-specific antibody titers were obtained prior to the 2nd and 3rd vaccination to assess primary and secondary antibody responses. Clinical protection status (anti-hepatitis B surface antigen immunoglobulin G ≥ 10 mIU/ml) was assessed 6 mo after the final immunization. Regression analyses revealed that shorter actigraphy-based sleep duration was associated with a lower secondary antibody response independent of age, sex, body mass index, and response to the initial immunization. Shorter sleep duration, measured by actigraphy and sleep diary, also predicted a decreased likelihood of being clinically protected from hepatitis B at the conclusion of the vaccination series. Neither sleep efficiency nor subjective sleep quality were significant predictors of antibody response. CONCLUSIONS: 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.