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Very little research has assessed how measures of negative and positive affect (NA and PA) derived from assessments at multiple time points per day (e.g., via ecological momentary assessment [EMA]), as opposed to questionnaires that rely on recall over a longer period, are related to levels of peripheral inflammation. We examined how different indicators of NA and PA predicted concentrations of C-reactive protein (CRP) and seven peripheral inflammatory cytokines (IL-1β, IL-6, TNF-α, IL-8, IL-4, IL-10, and IFN-γ) that were examined in the form of an inflammatory composite. A community-based sample of 220 adults (62% Black/African-American and 25% Hispanic/Latino; aged 25–65; 65% female) completed questionnaires at baseline (including recalled affect “over the past month”) and then provided EMA reports 5x/day for 14 days. Blood was drawn from each participant after completion of EMA and used to determine plasma levels of CRP and cytokines. Analyses examined if indicators of affect predicted inflammation, controlling for age, gender, body mass index, education, health conditions, and statin use. Neither recalled NA or PA nor momentary NA or PA (aggregated across the 14 days of EMA) were significantly associated with the cytokine composite or CRP. Negative mood more proximal to the blood draw (i.e., aggregated momentary NA in week 2 of EMA) was associated with the cytokine composite but not CRP. Exploratory moderation analyses revealed that the cytokine composite was also associated with PA in week 2 for men only, and with recalled NA for those with lower education. Exploratory analyses around temporal dynamics suggested that the timing of NA measurement relative to the blood draw mattered: Specifically, there were stronger trends of association between momentary NA and inflammatory cytokines when NA was assessed closer in time to blood collection. Future investigation of the relevance of temporal proximity and other measurement details may improve understanding of how affect relates to inflammation.

Although research has linked stress to depression and inflammation, the extent to which gender alters relationships between stress, depression, and inflammation is relatively unknown. In theory-driven exploratory analyses based on recent work (Majd et al., 2018), depressive affect was investigated as a statistical mediator of stress and inflammation in cross-sectional data; gender was examined as a moderator in this model. Participants (n = 162; 25–65 years old; 67% women; 87% non-white) reported depressive symptoms (PROMIS short-form), recent stressors (life events [past year]; perceived stress [past month]), and cumulative stress severity from EMA (past 2 weeks), and lifetime stressors. Inflammatory responses were determined from lipopolysaccharide (LPS) stimulated cytokines in blood collected at the end of the EMA period. Recent stress and inflammatory responses were indirectly linked via depressive symptoms; gender significantly moderated the depression-immune path (IL-6: w = 0.070, 95%CI[0.02, 0.15]; IL-10: w = 0.059, 95%CI[−0.004, 0.13]; TNF α : w = 0.064, 95%CI[0.02, 0.13]). Recent stress related to greater depressive symptoms for men and women; greater depressive symptoms in turn related to higher inflammatory responses in men, but reduced responses in women. Similar patterns were evident for other recent stress measures; weaker effects were evident for lifetime stress measures. This research suggests that the relationship between recent stress and stimulated inflammatory responses may be accounted for by depressive symptoms, and that the direction of the relationship between depression and inflammation may be dependent on gender.

Increasing evidence suggests that depression is linked with immune dysregulation. In this study, we examined the links between depressive symptoms and both basal and lipopolysaccharide-stimulated (ex vivo) levels of pro-inflammatory (IL-1beta, IL-6, IL-8, TNF-alpha) and anti-inflammatory (IL-10) cytokines in blood. Subjects were recruited from the Bronx NY and were socio-economically and racially diverse (ages 25–65). Exclusion criteria included inflammation-related illness and use of immunosuppressive drugs, resulting in 148 participants (97 women). On average the sample reported mild depressive symptoms (assessed using the PROMIS depression short-form scale). Regression analyses controlled for age, BMI, income, education, race/ethnicity, use of anti-inflammatory agents and antidepressants. No relationships between basal inflammatory levels and depressive symptoms were observed. However, in stimulated blood, a significant interaction of depressive symptoms by gender was observed, such that in women higher depressive scores were associated with lower production of TNF-alpha (p .80). Overall, higher depressive symptoms related to lower, possibly blunted, responses to endotoxin challenge in women, and higher, possibly exaggerated, responses in men. These findings provide evidence for gender differences in patterns of inflammatory dysregulation in individuals with greater depressive symptoms. Studying stimulated inflammatory biomarkers in gender stratified groups may clarify the links between inflammation and depression.

We examined whether peripheral inflammatory markers were better predicted by negative and positive affect (NA and PA) measures derived from ecological momentary assessment (EMA) in daily life, as compared to standard recall “over the past month” questionnaire. Diverse adult participants ( N = 206) completed questionnaires and then EMAs 5x/day for 14 days; blood was drawn afterwards, from which levels of IL-1beta, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, TNF-alpha, IFN-gamma, GM-CSF, and hsCRP were determined. Analyses controlled for BMI, age, gender, income, marital status, race/ethnicity, health conditions, and use of statins/anti-depressants. NA and PA derived from standard recall were not related to any biomarker. EMA reports were aggregated across each of the two weeks; Week 1 affect was not associated with any biomarker, but week 2 NA (more proximal to the blood draw) was associated with higher levels of every cytokine except IL-5 and IL-1beta (ps.01 to .001) and week 2 PA was associated with lower IL-6 ( p

Growing evidence suggests that positive emotions are protective against inflammation, yet less is known about the role of day-to-day positive experiences in inflammatory processes. This research examined the frequency of momentary positive events in relation to circulating inflammatory markers and stimulated inflammatory responses (ex vivo to an endotoxin challenge). In a racially diverse sample of 164 adults ages 26–65, positive events were measured 5 times per day for 14 days using smartphone-based momentary assessments. Blood was collected at the end of this 14-day period and assayed for pro-inflammatory cytokines (interleukin[IL]-6, IL-8, and TNF-alpha), anti-inflammatory cytokine IL-10, and lipopolysaccharide (LPS)-stimulated inflammatory responses. The frequency of momentary positive events was unrelated to circulating IL-6, IL-8, IL-10, and TNF-alpha, controlling for sociodemographics, body mass index, comorbid conditions, menopause, and tobacco and alcohol use. However, people who experienced more frequent positive events showed lower stimulated production of log IL-6 (fully-adjusted B = −0.20, SE = 0.10, p = 0.044) and log TNF-alpha (B = −0.30, SE = 0.09, p = 0.002), but not significantly lower stimulated log IL-8 (B = −0.18, SE = 0.11, p = 0.105) or log IL-10 (B = −0.27, SE = 0.17, p = 0.106). These findings suggest that minor positive events in daily life, although unrelated to basal inflammatory state, may confer salutary benefits by reducing inflammatory responses to an immune challenge.