Stimulated production of interleukin-8 covaries with psychosocial risk factors for inflammatory disease among middle-aged community volunteers

A growing literature suggests that psychosocial factors, such as chronic stress and depression, are associated with increased vulnerability to inflammatory disease; however, the mechanisms of this effect remain unclear. One possibility is that these psychosocial characteristics are associated with activation of innate inflammatory pathways. Here, we explore relationships between a range of psychosocial risk factors for inflammatory disease and a measure of inflammatory potential, lipopolysaccharide-induced production of the monocyte-derived proinflammatory cytokines/chemokines interleukin (IL)-1β, IL-6, TNF-α, and IL-8 among a community sample of 183 healthy adults aged 30–54 years. After controlling for demographic factors, health behavior practices, blood pressure, and white blood cell count, hierarchical regression analyses revealed a positive relationship between production of IL-8 and symptoms of depression, trait negative affect, and perceived stress. In contrast, there was an inverse relationship between IL-8 production and perceived social support. Relationships between IL-8 and symptoms of depression and perceived stress were attributable primarily to dispositional differences in NA. The relationship between negative affect measures and IL-8 was independent of social support. Although there were significant univariate associations between higher IL-6 production and symptoms of depression and less social support, these relationships did not withstand adjustment for demographic controls. There were no significant associations between IL-1β or TNF-α and any of the psychosocial parameters. Our findings suggest that individuals at greater psychosocial risk for the development of inflammatory diseases, including cardiovascular disease, also show greater stimulated production of the proinflammatory chemokine, IL-8. Further exploration of this potential psychophysiological pathway is warranted.