Psychological stress elicits not only an immune but also an autonomic and neuroendocrine response, and these responses have a discernible impact on immune function. In research examining the relationships among autonomic, neuroendocrine, and immune responses to stress, we found that sympathetic reactivity to psychological stress (as indexed by pre-ejection period, or PEP) predicted poorer T-cell response to influenza vaccination, r¼:68, p<:05, in a sample of older women(Cacioppo et al., 1998). Women who were high sympathetic reactors also exhibited elevated antibody titers to EBV (Cacioppo et al., 2002a), consistent with the notion that exaggerated sympathetic responses to stress are associated with diminished cellular immunity. Importantly, PEP responses to stress among these older women appear consistent across acute psychological tasks (Hawkley et al., 2001) and stable over time (Burleson et al., 2002), suggesting that sympathetic reactivity to everyday stressors and hassles may represent one mechanism by which stress affects immune function.Sympathetic nervous system activity increases with age (Seals and Esler, 2000), and this may exacerbate stressrelated immune decrements. The exact mechanism linking exaggerated sympathetic activity and immune decrements is an active area of investigation, but Friedman and Irwin (1995) provide evidence consistent with sympathetic mediation of corticotrophin releasing hormone (CRH) effects, and suggest that abnormal CRH regulation in the brain of the elderly may produce both age-related increases in sympathetic activity and decreases in immune functioning.
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