Age, stress, and markers of inflammation among middle-aged to older African American adults: Findings from The Heart of Detroit Study

BACKGROUND: Aging is associated with increasing systemic inflammation (inflammaging) alongside declining immune function (immunosenescence); stress is hypothesized to exacerbate these effects. However, whether stress and age interact to effect inflammatory markers among African Americans is unknown. We hypothesized that stress would amplify age-related changes in inflammation and immune function, such that greater stress would result in greater circulating and lower stimulated markers of inflammation at greater ages. METHODS: Data are from The Heart of Detroit Study (n = 522 African Americans aged 55-75 years). Analyses included 312 participants who provided usable blood samples and had C-reactive protein (CRP) < 10 mg/L. Markers of basal inflammation [interleukin (IL)-6, IL-8, IL-10, tumor necrosis factor (TNF)-α, macrophage migration inhibitory factor (MIF), CRP] and ex vivo lipopolysaccharide-stimulated inflammation (IL-1β, IL-6, IL-8, IL-10, TNF-α) were assessed. Main effects of perceived stress and age on inflammatory markers were tested with linear regression; an interaction term was then added to assess moderation. Significant interactions were probed with simple slopes analyses. RESULTS: Age and stress interacted to affect the basal cytokine composite score, IL-8, and MIF, but not the stimulated composite score or CRP. Among participants with average to high stress, greater age was associated with higher basal cytokine composite scores; with high stress, greater age was also associated with higher IL-8. With low stress, greater age was associated with lower MIF. CONCLUSION: Results suggest that moderate to high perceived stress exacerbates inflammaging. No such effect on stimulated inflammation was observed. Intriguingly, low stress may protect against inflammaging.