Vogelzangs · Translational psychiatry 2016 · cross-sectional case-control study · n=1242

Cytokine production capacity in depression and anxiety.

Cited 199 times in the scientific literature.

Level 4 - case-series / case-control

Cross-sectional observational comparison of clinical groups and healthy controls.

PubMed 27244234 · doi:10.1038/tp.2016.92 · record verified 2026-08-27

What was done

Baseline data from the Netherlands Study of Depression and Anxiety (NESDA) were analyzed across three groups aged 18–65 years (66% women): current DSM-IV depressive or anxiety disorders (n=591), remitted disorders (n=354), and healthy controls (n=297). Depressive and anxiety symptoms were assessed using the Inventory of Depressive Symptomatology (IDS) and the Beck Anxiety Inventory (BAI). Whole blood was stimulated ex vivo with lipopolysaccharide (LPS) to measure the production capacity of 13 cytokines, and basal plasma levels of C-reactive protein, IL-6, and TNF-α were also measured.

What was found

Unadjusted LPS-stimulated inflammation and basal inflammation were both associated with higher odds of current depressive/anxiety disorders (OR=1.28, P=0.009 and OR=1.28, P=0.001, respectively). After adjusting for lifestyle and health variables, these overall diagnostic associations became non-significant (OR=1.13, P=0.21 for LPS; OR=1.07, P=0.45 for basal). However, specific LPS-stimulated IL-8 production remained associated with both remitted (OR=1.25, P=0.02) and current disorders (OR=1.28, P=0.005). Furthermore, LPS-stimulated inflammation correlated with depressive (β=0.129, P<0.001) and anxiety (β=0.165, P<0.001) symptom severity; after full adjustment, LPS-stimulated cytokine capacity remained significantly associated with anxiety symptom severity (BAI: LPS index, IL-6, IL-8, IL-10, IL-18, MCP-1, MMP2, TNF-β) and specific depressive symptoms (IDS: IL-8, MCP-1, MMP2).

Why it matters

This study shows that innate cytokine production capacity, particularly for IL-8, tracks with anxiety and depressive symptom severity independently of lifestyle and health confounders, suggesting immune reactivity may represent an underlying vulnerability rather than purely a secondary byproduct of unhealthy behaviors.

Limits

The study is cross-sectional, preventing causal conclusions about whether altered cytokine reactivity causes or results from mood pathology. Detailed breakdown of specific medications, exact timing of blood sampling, and potential unmeasured lifestyle confounders were not fully accounted for in the reported abstract.

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