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Bereavement is a common life event for older adults and is associated with increased risk of morbidity and mortality, though the underlying reasons for this link are poorly understood. Although physical and emotional stressors and ageing are known to suppress immunity, few studies have explored the impact of bereavement upon immunity in the older population. We therefore hypothesised that the emotional stress of bereavement would suppress immune function, specifically neutrophil bactericidal activity, in older adults. A between-subjects design was used to examine the effect of recent bereavement (2 months) on neutrophil function in elders. Participants were 24 bereaved and 24 age- and sex-matched non-bereaved controls all aged 65+ years. Neutrophil phagocytosis of Escherichia coli (E. coli) and stimulated superoxide production were assessed. Cortisol and dehydroepiandrosterone-sulphate (DHEAS) levels were determined in serum to assess potential mechanisms. Depressive and anxiety symptoms were measured by questionnaire. Neutrophil superoxide production was significantly reduced among the bereaved when challenged with E. coli (p=0.05), or phorbol 12-myristate 13-acetate (p=0.009). Further, the bereaved group had a significantly higher cortisol:DHEAS ratio compared to controls (p=0.03). There was no difference in neutrophil phagocytosis between the two groups. The psychological questionnaire results showed that the bereaved had significantly greater depressive and anxiety symptoms than the non-bereaved. The emotional stress of bereavement is associated with suppressed neutrophil superoxide production and with a raised cortisol:DHEAS ratio. The stress of bereavement exaggerates the age-related decline in HPA axis and combines with immune ageing to further suppress immune function, which may help to the explain increased risk of infection in bereaved older adults.

Objective: To examine the effects of an acute laboratory psychological stress task on neutrophil function, specifically phagocytosis of Escherichia coli and stimulated superoxide production in human neutrophils. There is mounting evidence that acute stress is associated with short-term increases in a number of immune indices. Methods: Participants were 40 (n = 20 females) university students (mean age, 25.9 ± 4.56 years). Blood samples to determine neutrophil function by flow cytometry were taken at the end of resting baseline, during an acute stress task, and during recovery. The stress task was a 10-minute time-pressured mental arithmetic challenge with social evaluation. Results: There was an acute increase in phagocytic ability, \(\rho\) = .047, η2p = 0.076, and a reduction of superoxide production, p = .026, η2p = 0.101, associated with the stress task relative to baseline. Conclusion: These findings suggest that neutrophil bactericidal function may be sensitive to mental challenge tasks that provoke acute psychological stress. Further research is needed to replicate the observed psychological stress-induced changes in neutrophil function.

The innate or non-specific immune system consists of soluble components, namely the complement system and cellular elements. The latter includes neutrophils, which make up the majority of the innate immune cells in circulation, and deal with rapidly dividing bacteria. This chapter will focus on the influence of psychological stress and ageing on neutrophil numbers and function. Neutrophils are a major component of innate immunity and are the dominant leukocyte in the circulation, making up 60 % of the white cell count. They are also the shortest lived blood cell, dying by apoptosis approximately 24 h after leaving the bone marrow (Savill et al., J Clin Invest 83:865–875, 1989; Scheel-Toellner et al , Biochem Soc Trans 32:461–464, 2004). These cells play a crucial role in killing invading pathogens, particularly rapidly dividing bacteria, and are key cellular components of the early phase of inflammatory responses (Nathan et al., Nat Rev Immunol 6:173–182, 2006). Neutrophils act quickly and without specificity, although their bacterial recognition systems are many and complex. Neutrophils are recruited to sites of infection via chemical homing (chemotactic) signals, such as the chemokine CXCL8 (also known as IL8). Once in contact with the pathogen they uptake the microbe by engulfing (phagocytosis) mediated via opsonic receptors that detect complement proteins C3b and C3Bi or antibody coating the microbe.

Ageing is associated with higher morbidity and mortality, and declining immune function, termed immunesenescence. The present study examined the effects of an acute laboratory psychological stress task on innate immunity, specifically neutrophil function, among older adults. The two functional assays used were phagocytosis of Escherichia coli and stimulated superoxide production. Participants were 17 (11 female) older adults (mean age 75.7, SD = 7.06 years). Blood samples to determine neutrophil function by flow cytometry were taken at the end of resting baseline, during an acute stress task and during recovery. The stress task was an 8-minute time-pressured mental arithmetic challenge with social evaluation. There was a significant reduction in neutrophil superoxide production, p = .017, η 2 p = .240, associated with the stress task relative to baseline, but no effect on phagocytosis. The results of this study could contribute to explaining the increased risk of infection in older adults, particularly those subject to frequent stress exposures. Future research is needed to explore the underlying mechanisms of acute stress effects on human neutrophil function in older adults in greater detail.