A total of 513 patients were included.Cross-sectional associations were found between HsCRP and depressive symptoms at baseline (β = 0.9, confidence interval [CI] = 0.4-1.4) and 6-month follow-up (β = 1.1, CI = 0.3-2.0), and between IL-1β and depressive symptoms at 6-month follow-up (β = 1.3, CI = 0.8-1.8) and 12-month follow-up (β = 1.2, CI = 0.4-1.9).
Gender (β = .177, P = .035), income (β = -.252, P = .004), whether the patient's income met their basic needs (β = .180, P = .035), and IL-1β (β = -.165, P = .045) independently predicted depressive symptoms and together explained 19.4% of variance associated with depressive symptoms.
To provide more evidence, we measured the plasma levels of IL-1β, IL-6, interferon (INT)-α2, INT-γ, and tumor necrosis factor (TNF)-α in patients having MDD and explored correlations between the five proinflammatory cytokines and specific depressive symptoms.
For T2D, hsCRP, IL-1RA, CCL2 and adiponectin or its isoforms were associated with depressive symptoms in at least two studies, whereas positive associations of IL-1β, IL-6 and IL-18 with depressive symptoms or depression were reported from single cohorts.
In contrast, IL-6, CRP, and IL-1β did not demonstrate statistically significant associations with depressive symptoms by the EPDS in either crude or adjusted models.
In patients with T2D, reductions in depressive symptoms were associated with reductions in high-sensitivity C-reactive protein (hsCRP), interleukin (IL)-18 and IL-1 receptor antagonist (IL-1RA) (P ≤ 0.016), whereas no associations were seen for IL-6, CCL2 and adiponectin.
Strong statistical evidence was provided for interactions between: 1) IL-1β (rs1143634) and fear of pain for predicting loss of shoulder flexion and abduction, 2) IL-1β (rs1143634) and anxiety for predicting loss of flexion, and 3) IL-1β (rs1143634) and depressive symptoms for predicting loss of internal rotation.
This study revealed the potential therapeutic effects of fluoxetine by reducing central and peripheral levels of IL-1β in the alleviation of depressive symptoms.
The aim of the present study was to investigate a trio of functional SNPs in the promoter regions of IL6 (-174G>C, rs1800795), IL1β (-511C>T, rs16944), and TNF (-308G>A, rs1800629) as moderators of the relationship between chronic stress exposure and elevations in depressive symptoms.
Results from the recruited cohort (n = 190) indicated strong statistical evidence for the interactions between 1) TNF/LTA SNP rs2229094 and depression symptoms for average pain intensity and duration and 2) IL1B two SNP diplotype and kinesiophobia for average shoulder pain intensity.