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.
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.
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.
Furthermore, mGluR5 deficiency dramatically inhibits cytokines release from bone marrow cells, such as IL-1β, TNF-α and IL-6, alleviating proinflammatory responses in LPS-induced depression model.
The biological link between depression, inflammation, and CVD can be related to high levels of pro-inflammatory cytokines, such as IL-1β, TNF-α, and IL-6, released by macrophages which play a central role in the pathophysiology of both depression and CVD.
In the rat model and human cirrhosis a proinflammatory cytokine pattern (elevation of interferon gamma, interleukin [IL]-1β, IL-6) was registered which in humans correlated to the degree of HE and depression.
Considering the inflammatory-depression link, and that women are twice as likely to experience depression compared to men, the current study (<i>N</i> = 475 university students) examined the moderating role of three independent cytokine single nucleotide polymorphisms (SNPs; IL-1βrs16944, IL-6 rs1800795 SNP, TNF-α rs1800629) in the relationship between early-life adversity and depressive symptoms, and whether these relations differed between males and females.
Elevations in brain interleukin-1 beta (IL-1β) during chronic stress exposure have been implicated in behavioral and cognitive impairments associated with depression and anxiety.
In all subjects, the IL-1β levels were correlated with PCL scores, after controlling for covariates, including age, education, marital status and gender, trauma exposure severity and depression.
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 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.
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.
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.
Finally, the effects of chronic stress on both depression- and anxiety-like behaviors can be mimicked by exogenous intracerebroventricular (i.c.v.) administration of IL-1β in both WT and Caspase-1<sup>-/-</sup> mice.
In conclusion, the results of the present study suggested that AT-I exerts anti-depressant-like effects in a CUMS-induced model of depression in mice, the molecular mechanism of which is associated with the inhibition of NLRP3 inflammasome activation to decrease IL-1β production.
Incident depression was significantly associated with increases in IL-1β, IL-6, and IL-8 levels during the follow-up independent of relevant covariates and after applying Bonferroni corrections.
Although the IL-1 molecules are traditionally considered to be classical proinflammatory cytokines, their functions are not restricted to inflammation, and they have also been shown to play a key role in a wide range of additional physiological and pathological functions, including learning modulation, sleep, pregnancy, depression, appetite, hematopoiesis, metabolism, and many others.