Here we use homozygous and heterozygous transgenic mice expressing elevated levels of IL-6 in the CNS due to increased astrocyte expression and non-transgenic littermates to examine a role for astrocyte-produced IL-6 in emotionality (response to novelty, anxiety-like, and depressive-like behaviors).
On T2, self-reported doctors' empathy ability was significantly positively correlated with patient sleep and self-efficacy (P<0.01), and significantly negatively correlated with patient anxiety and IL-6 (P<0.01).
Our findings thus suggested that the differential expressions of BDNF and IL-6 after CSDS may contribute to less anxiety and less despair observed in GHS-R1a-deficient mice than in WT control mice.
Covariance analysis showed that mood disorders alone, increase both interleukin levels (IL-6, p = 0.019; and IL-10, p = 0.026), whilst the interaction of mood disorders and suicide risk or anxiety disorders did not.
After controlling for demographic characteristics, body mass index, and depressive symptoms, attachment avoidance and anxiety were associated with IL-6 but not CRP.
The values for the following parameters decreased in the hypertensive group post training: anxiety (-6.2 ± 2 score; 60%), Timed Up and Go test (-7.4 ± 0.3 sec; 30%), protein carbonylation (-0.15 ± 0.03 nmol/mg protein; 50%), nitric oxide (12.4 ± 6 nmol/mg protein; 62%), interleukin-6 (-27.6 ± 5.7 pg/mg protein; 46%), and tissue necrosis factor-alpha (-52.4 ± 3.8 pg/mg protein; 40%); however, the values of the following parameters increased before training: Berg score (56 ± 2; 7.8%), flexibility (27 ± 1 cm; 71%); glutathione (3.1 ± 1.3 nmol/mg protein; 138%), and superoxide dismutase (1.6 ± 0.4 nmol/mg; 166%).
Next, treatments with fecal microbiota of ampicillin-treated mouse (FAP), K. oxytoca, or lipopolysaccharide isolated from K. oxytoca (KL) induced anxiety and colitis in mice and increased blood corticosterone, IL-6, and lipopolysaccharide levels.
The changes of BPRS-E-manic and BPRS-E-anxiety scores correlated with the baseline IL-1ra (r=-0.393), IL-6 (r=-0.407), and insulin like growth factor binding protein 3 (r=-0.446).
Migraine patients showed higher tension (p=0.019) and anxiety scores (p=0.046), TNF-α (p<0.01), and IL-12p70 (p=0.01), while IL-6 (p<0.01), IL-8 (p<0.01), and IL-10 (p<0.01) were decreased compared to control group.
Establish whether inflammatory biomarkers-serum amyloid A (SAA), C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α)-are related to key symptoms of depression, including anxiety and fatigue, in a cross-sectional, out-patient setting to identify biomarkers that reflect psychiatric symptomatology in a naturalistic, real-life population.
The present study suggests that changes in the GSH-dependent defense system, NF-κB activation and increased IL-6 protein expression may have a role in social isolation-induced changes in a rat model of depression and anxiety, and contributes to our understanding of the mechanisms that underlie the antidepressant and anti-inflammatory activity of Flx in socially isolated rats.
However, the expression of DNMT1/3A, EZH2 and IL-6 genes increases with increasing Hospital Anxiety and Depression Scale-Anxiety scores in the anxious cohort only.
During antiviral treatment we reported that subjects with CC genotype (IL-6) presented significantly lower changes from baseline in IFN-induced depression (p=0.005) and IFN-induced anxiety (p=0.004).