Correlation analysis between HADS score and cytokine serum levels revealed positive associations of anxiety and/or depression with IL-1β, IL-6, IL-8, and TNF-α, and a negative correlation with IL-10, suggesting that cytokines are involved in the pathophysiology of these psychological disorders in CRC patients.
The main findings of this study indicate a functional network in which several IL-1β-related molecules in CSF influence fatigue in addition to the classical clinical factors of depression and pain.
Then, alterations of pro-inflammation cytokine IL1-β level and microglia activity in the hypothalamus, which are involved in the pathophysiology of depression, were examined.
The results of this study suggest that palmatine can alleviate the comorbidity of DNP and DP by inhibiting the expression of P2X<sub>7</sub> receptors in the hippocampus, and its action may be related to suppression of the phosphorylation of ERK1/2 and the release of TNF-α and IL-1β in the hippocampus.
Several lines of evidence indicate that brain cytokines, principally interleukin-1beta (IL-1beta) and IL-1 receptor antagonist may have a role in the biology of major depression, and that they might additionally be involved in the pathophysiology and somatic consequences of depression as well as in the effects of antidepressant treatment.
These findings are consistent with a previously reported association between reduced serum IL-1β levels and reduced depression severity following 12 weeks of physical exercise in 105 depressed adults.
The hippocampus is particularly vulnerable to increases in the pro-inflammatory cytokine interleukin-1β (IL-1β), a mediator of neuroinflammation, with elevated levels implicated in the aetiology of neurodegenerative diseases such as Alzheimer's and Parkinson's, and in stress-related disorders such as depression.
Correlation analysis revealed that depression severity negatively correlated with IL-12 in males, and positively correlated with IL-1β and tumor necrosis factor (TNF)-α in females.
TNF-α -308G/A and IL-8 -251T/A were significantly associated with AD and IL-1β +3953C/T with late-life depression, while the significance of these associations was lost after Bonferroni correction.
In this study, we tested the leukocyte mRNA expression levels of genes belonging to glucocorticoid receptor (GR) function (FKBP-4, FKBP-5, and GR), inflammation (interleukin (IL)-1α, IL-1β, IL-4, IL-6, IL-7, IL-8, IL-10, macrophage inhibiting factor (MIF), and tumor necrosis factor (TNF)-α), and neuroplasticity (brain-derived neurotrophic factor (BDNF), p11 and VGF), in healthy controls (n=34) and depressed patients (n=74), before and after 8 weeks of treatment with escitalopram or nortriptyline, as part of the Genome-based Therapeutic Drugs for Depression study.
The hippocampus is particularly vulnerable to altered concentrations of the pro-inflammatory cytokine interleukin-1β (IL-1β), with elevated levels implicated in the aetiology of neurodegenerative disorders such as Alzheimer's and Parkinson's, and stress-related disorders such as depression.
In the rat depression model, depression decreased tear secretion and increased IL-1β and TNF-α production, whereas the serotonin, TLR2, and TLR4 levels were not increased.
Since IL-1β and PGE<sub>2</sub> increase in serum of stressed patients and potentially trigger depression, we used an animal model of chronic unpredictable stress (CUS) to investigate the potential impact of LTB<sub>4</sub> over depression-like symptoms.
Our findings suggest that the IL1B-511C/T polymorphism may be related to age at manifestation among individuals vulnerable to depression, but they do not affect the basic vulnerability to or severity of depression in elderly Chinese adults.
Patients who were symptomatic had the highest depression and anxiety scores, together with increased intestinal expression of IL-1β, IL-6 and matrix metalloproteinase-9, increased circulating IL-6 and CRP, and an increased circulating kynurenine:tryptophan ratio.
The logistic regression model and ROC curves based on serum levels of BDNF, IL-1β, and cortisol could distinguish depression from TDS in early stage, which could provide assistance to the differential diagnosis of geriatric depression and TDS.