Depressive symptoms and inflammatory cytokines in women with preterm and term delivery

2010 ◽  
Vol 24 ◽  
pp. S12
Author(s):  
E. Fransson ◽  
A. Hjelmstedt ◽  
A. Dubicke ◽  
B. Byström ◽  
M. Lekander ◽  
...  
Keyword(s):  
Depressive Symptoms ◽  
Inflammatory Cytokines ◽  
Term Delivery

scholarly journals Plasma inflammatory cytokines and treatment-resistant depression with comorbid pain: improvement by ketamine

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Yanling Zhou ◽  
Chengyu Wang ◽  
Xiaofeng Lan ◽  
Hanqiu Li ◽  
Ziyuan Chao ◽  
...  
Keyword(s):  
Depressive Symptoms ◽  
Individual Differences ◽  
Inflammatory Cytokines ◽  
Treatment Resistant Depression ◽  
Treatment Resistant ◽  
Pain Group ◽  
Gm Csf ◽  
Tnf Α ◽  
Antidepressant Effects ◽  
Resistant Depression

Abstract Background Treatment-resistant depression (TRD) and pain frequently coexist clinically. Ketamine has analgesic and antidepressant effects, but few studies have evaluated individual differences in antidepressant outcomes to repeated ketamine in TRD patients with comorbid pain. Our aims were to determine the difference in ketamine’s antidepressant effects in TRD patients with or without pain and then to examine whether inflammatory cytokines might contribute to ketamine’s effect. Methods Sixty-six patients with TRD received six infusions of ketamine. Plasma levels of 19 inflammatory cytokines were assessed at baseline and post-infusion (day 13 and day 26) using the Luminex assay. Plasma inflammatory cytokines of sixty healthy controls (HCs) were also examined. Results TRD patients with pain had a higher antidepressant response rate (χ2 = 4.062, P = 0.044) and remission rate (χ2 = 4.062, P = 0.044) than patients without pain. Before ketamine treatment, GM-CSF and IL-6 levels were higher in the pain group than in the non-pain and HC groups. In the pain group, levels of TNF-α and IL-6 at day 13 and GM-CSF, fractalkine, IFN-γ, IL-10, MIP-3α, IL-12P70, IL-17α, IL-1β, IL-2, IL-4, IL-23, IL-5, IL-6, IL-7, MIP-1β, and TNF-α at day 26 were lower than those at baseline; in the non-pain group, TNF-α levels at day 13 and day 26 were lower than those at baseline. In the pain group, the changes of IL-6 were associated with improvement in pain intensity (β = 0.333, P = 0.001) and depressive symptoms (β = 0.478, P = 0.005) at day 13. Path analysis showed the direct (β = 2.995, P = 0.028) and indirect (β = 0.867, P = 0.042) effects of changes of IL-6 on improvement in depressive symptoms both were statistically significant. Conclusion This study suggested that an elevated inflammatory response plays a critical role in individual differences in TRD patients with or without pain. Ketamine showed great antidepressant and analgesic effects in TRD patients with pain, which may be related to its effects on modulating inflammation. Trial registration ChiCTR, ChiCTR-OOC-17012239. Registered on 26 May 2017

scholarly journals Inflammation in Depression

2021 ◽  
Vol 10 (2) ◽  
pp. 50
Author(s):  
Novi Agung Rahmawati ◽  
Azimatul Karimah ◽  
Mustafa M Amin
Keyword(s):  
Depressive Symptoms ◽  
Inflammatory Cytokines ◽  
Clinical Studies ◽  
Chronic Condition ◽  
Current Understanding ◽  
Neurotransmitter Systems ◽  
Treatment Of Depression ◽  
Pro Inflammatory Cytokines

Depression is a chronic condition that imposes a substantial burden of disability globally. Three principal neurotransmitters (norepinephrine (NE), dopamine (DA), and serotonin (5-HT)) implicated the pathophysiology and treatment of depression. Clinical studies have found a significant association between numerous pro-inflammatory cytokines with depressive symptoms, endocrine, and neurotransmitter systems. Here, we detail our current understanding about the role of inflammation in depression, the mechanisms that are involved, and show how it is possible to innovate and develop new therapeutics of depression in the field of neuroinflammation.

scholarly journals Pro-Inflammatory Cytokines: Potential Links between the Endocannabinoid System and the Kynurenine Pathway in Depression

2021 ◽  
Vol 22 (11) ◽  
pp. 5903
Author(s):  
Ferenc Zádor ◽  
Sâmia Joca ◽  
Gábor Nagy-Grócz ◽  
Szabolcs Dvorácskó ◽  
Edina Szűcs ◽  
...  
Keyword(s):  
Depressive Symptoms ◽  
Inflammatory Cytokines ◽  
Synthetic Cannabinoids ◽  
Endocannabinoid System ◽  
Kynurenine Pathway ◽  
Tryptophan Depletion ◽  
The Past ◽  
Cytokine Levels ◽  
Inflammatory Component ◽  
Pro Inflammatory Cytokines

Substance use/abuse is one of the main causes of depressive symptoms. Cannabis and synthetic cannabinoids in particular gained significant popularity in the past years. There is an increasing amount of clinical data associating such compounds with the inflammatory component of depression, indicated by the up-regulation of pro-inflammatory cytokines. Pro-inflammatory cytokines are also well-known to regulate the enzymes of the kynurenine pathway (KP), which is responsible for metabolizing tryptophan, a precursor in serotonin synthesis. Enhanced pro-inflammatory cytokine levels may over-activate the KP, leading to tryptophan depletion and reduced serotonin levels, which can subsequently precipitate depressive symptoms. Therefore, such mechanism might represent a possible link between the endocannabinoid system (ECS) and the KP in depression, via the inflammatory and dysregulated serotonergic component of the disorder. This review will summarize the data regarding those natural and synthetic cannabinoids that increase pro-inflammatory cytokines. Furthermore, the data on such cytokines associated with KP activation will be further reviewed accordingly. The interaction of the ECS and the KP has been postulated and demonstrated in some studies previously. This review will further contribute to this yet less explored connection and propose the KP to be the missing link between cannabinoid-induced inflammation and depressive symptoms.

scholarly journals Plasma Inflammatory Cytokines and Depressed Patients With Comorbid Pain: Improvement by Ketamine

2021 ◽  
Author(s):  
Yanling Zhou ◽  
Chengyu Wang ◽  
Xiaofeng Lan ◽  
Hanqiu Li ◽  
Ziyuan Chao ◽  
...  
Keyword(s):  
Depressive Symptoms ◽  
Individual Differences ◽  
Inflammatory Cytokines ◽  
Pain Group ◽  
Gm Csf ◽  
Luminex Assay ◽  
Analgesic Effects ◽  
Depressed Patients ◽  
Antidepressant Effects ◽  
The Difference

Abstract Background: Depression and pain frequently coexist clinically. Ketamine has analgesic and antidepressant effects, but few studies have evaluated individual differences in antidepressant outcomes to repeated ketamine in depressed patients with comorbid pain. Our aims were to determine the difference in ketamine’s antidepressant effects in depressed patients with or without pain and then to examine whether inflammatory cytokines might contribute to ketamine’s effect. Methods: Seventy-eight patients with major depressive disorder received six infusions of ketamine. Plasma levels of 19 inflammatory cytokines were assessed at baseline and post-infusion (day 13 and day 26) using the Luminex assay. Plasma inflammatory cytokines of sixty healthy controls (HCs) were also examined. Results: At baseline, the levels of GM-CSF, IL-1β and IL-6 were higher in pain group than in non-pain and HC groups. Pain group had better antidepressant outcomes than non-pain group. Pain group showed a greater decrease in IL-6 at day 13 and a greater decrease in IL-10, MIP-3α, IL-1β, IL-5 and IL-6 at day 26 than non-pain group. In the pain group, the changes in IL-6 levels were associated with improvement in pain intensity (β=0.347, t=2.159, P=0.038) and depressive symptoms (β=0.590, t=4.201, P<0.001) at day 13. The Sobel test showed indirect effects between decreases in IL-6 levels and improvement in depressive symptoms (Z=2.026, P=0.043).Conclusion: This study suggested that an elevated inflammatory response plays a key role in individual differences in depressed patients with or without pain. Ketamine showed great antidepressant and analgesic effects in depressed patients with pain, which may be related to its anti-inflammatory effect.

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