Association of circulating immune cell phenotypes and peripheral inflammatory biomarkers with depressive symptoms in...

Depression is a common mental health disorder with substantial impact on older adults. Immune dysfunction has been studied as a mechanism for depressive symptoms, providing the opportunity for new targeted treatment approaches.

This study investigated the associations between immune cell phenotypes, determined by flow cytometry, and peripheral inflammatory biomarkers, measured using the OLINK Inflammation panel, with Center for Epidemiologic Studies Depression Scale (CES-D) scores, indicative of depressive symptoms, in the Framingham Heart Study Offspring Cohort. Regression models were used with proteins or immune cells as predictors and CES-D scores as the outcome, adjusting for age, sex, BMI, smoking status, CVD, depression medication use, NSAID use, and cytomegalovirus (CMV) status (immune cells only). We used Bonferroni adjusted p < 0.005 to declare significance. Effect estimates (beta) are reported in standard deviation units.

Participants (n = 831) had a mean age 61, were 52 % female, and had a mean CES-D score 5 (SD=7) with 8 % (n = 67) having a CES-D score > /= 16. Our results suggested a positive association between FGF-19 and CES-D score (beta=0.11, p = 0.004), as well as a suggestive negative trend between the CD8 +IL17 + :CD8 +CD25 +FoxP3 + ratio (CD8Tc17/CD8 +Tregs) and CES-D score (beta=-0.1, p = 0.03). In addition, we observed a positive suggestive trend between IL-17C and depressive symptoms (CES-D >/= 16) (beta=0.35 p = 0.009), that strengthened with higher levels of symptoms (p < 0.005).

The positive association between FGF-19 and depressive symptoms may suggest the contribution of metabolic and cognitive dysfunction to the pathophysiology of depression. The link between higher IL-17C levels and high CES-D score increased in strength as the cutoff point for a high CES-D score was increased, suggesting a link between IL-17C and more severe depressive symptoms. This study helps to expand our understanding of the role of inflammation in the pathophysiology of depression.