Inflammatory reactivity to acute laboratory stress is thought to reflect individual differences in responsivity to environmental stressors and may confer future health risk. To characterize this response, we conducted a meta-analysis of 34 studies that measured circulating inflammatory markers and 15 studies that measured stimulated production of inflammatory markers before and after exposure to laboratory challenge. Results showed significant stress-related increases in circulating interleukin (IL)-1β (d = 0.66, p < .001), IL-6 (d = 0.35, p < .001), IL-10 (d = 0.69, p < .001), and tumor necrosis factor(TNF)-α (d = 0.28, p < .001), but not IL-1ra, IL-2, interferon-γ, or C-reactive protein. There were sufficient data to assess the time course of IL-6, IL-1β, and TNF-α reactivity. IL-6 increased from baseline to measures taken 40–50, 60–75, 90, and 120 min following stress, with the largest effect at 90min post-stress (d = 0.70, p < .001). IL-1β increased from baseline to 20–30, 40–50, and 60–70 min following stress, with the largest effect between 40–50 min post-stress (d = .73, p = .02). For TNF-α, there was a significant increase from baseline to 31–50 min post stress (d = 0.44, p = .01), but not at later times. There was no difference in magnitude of IL-6 reactivity as a function of type of stress (social-evaluative versus other). For stimulated inflammatory markers, results showed stress-related increases in IL-1β when measured 20–120 min post-stress (d = 1.09, p < .001), and in IL-4 and interferon-γ when measured 0–10 min post stressor (d = −0.42, p < .001 and d = 0.47, p < .001). These results extend findings from a prior meta-analysis (Steptoe, Hamer, & Chida, 2007) to show reliable increases in circulating IL-6, IL-1β, IL-10 and TNF-α and stimulated IL-1β, IL-4 and interferon-γ in response to acute stress. It is possible that these responses contribute to associations between exposure to life challenges and vulnerability to inflammatory disease.

Negative emotions are reliably associated with poorer health (e.g., Kiecolt-Glaser, McGuire, Robles, & Glaser, 2002), but only recently has research begun to acknowledge the important role of positive emotions for our physical health (Fredrickson, 2003). We examine the link between dispositional positive affect and one potential biological pathway between positive emotions and health-proinflammatory cytokines, specifically levels of interleukin-6 (IL-6). We hypothesized that greater trait positive affect would be associated with lower levels of IL-6 in a healthy sample. We found support for this hypothesis across two studies. We also explored the relationship between discrete positive emotions and IL-6 levels, finding that awe, measured in two different ways, was the strongest predictor of lower levels of proinflammatory cytokines. These effects held when controlling for relevant personality and health variables. This work suggests a potential biological pathway between positive emotions and health through proinflammatory cytokines.

This research independently manipulated two potential attenuators of stereotype threat -reappraisal of anxiety and test framing -to explore their independent and combined effects. Female participants took a difficult math exam that was described as gender-biased or gender-fair and were told that anxious arousal could positively impact performance or were given no information regarding arousal. Levels of the cytokine Interleukin-6 (IL-6), an immune marker of inflammation, were measured in oral mucosal transudate (OMT) both before and after the exam. Our findings indicate that directing reappraisal of physiological arousal attenuated increases in IL-6 across test framing conditions, and was especially effective under stereotype threat (i.e., gender-biased test condition). Reappraisal also mapped onto better test performance in the threat condition. Together, these findings provide insight into the unique and interactive effects of two situational interventions meant to reduce stereotype threat, indexed here by both physiological and performance-based correlates of threat.

We experimentally tested whether negative stereotypes linked to lower socioeconomic status (SES), in addition to impairing academic performance (Croizet & Claire, 1998), instigate inflammation processes that are implicated in numerous disease processes. In Study 1, verbal test performance and activation of inflammation processes (measured by levels of an inflammatory protein, Interleukin-6 [IL-6]) varied as a function of SES and test framing (i.e., diagnostic vs. nondiagnostic of intellectual ability), with low SES students underperforming and exhibiting greater IL-6 production in the ''diagnostic'' condition. In Study 2, students expected their verbal exam performance to be compared to peers of higher or lower SES. Low SES students in the upward comparison condition displayed the greatest inflammatory response and worst test performance. Across both studies, different facets of SES predicted vulnerability to negative outcomes, such that low early life SES predicted heightened inflammation responses, while low current SES predicted impaired academic performance.

Inflammatory cytokine levels predict a wide range of human diseases, including depression, cardiovascular disease, type 2 diabetes, autoimmune disease, general morbidity, and mortality. Stress and social experiences throughout the lifecourse have been associated with inflammatory processes. We conducted studies in humans and laboratory rats to examine the effect of early life experience and adult social position in predicting IL-6 levels. Human participants reported family homeownership during their childhood and current subjective social status. Interleukin-6 (IL-6) was measured from oral mucosal transudate. Rats were housed in groups of three, matched for quality of maternal care received. Social status was assessed via competition for resources, and plasma IL-6 was assessed in adulthood. In both humans and rats, we identified an interaction effect; early social experience moderated the effect of adult social status on IL-6 levels. Rats that experienced low levels of maternal care and people with low childhood socioeconomic status represented both the highest and lowest levels of IL-6 in adulthood, depending on their social status as young adults. The predicted interaction held for non-Hispanic people, but did not occur among Hispanic individuals. Adversity early in life may not have a monotonically negative effect on adult health, but may alter biological sensitivity to later social experiences.