scholarly journals A role of innate immune molecules in behavioral changes induced by repeated social defeat stress in mice

Author(s):  
Xiang Nie ◽  
Shiho Kitaoka ◽  
Kohei Tanaka ◽  
Atsubumi Ogawa ◽  
Fumitake Nakano ◽  
...  
Author(s):  
Shiho Kitaoka ◽  
Xiang Nie ◽  
Kohei Tanaka ◽  
Atsubumi Ogawa ◽  
Fumitake Nakano ◽  
...  

2014 ◽  
Vol 232 (9) ◽  
pp. 1555-1569 ◽  
Author(s):  
Jasmine J. Yap ◽  
Elena H. Chartoff ◽  
Elizabeth N. Holly ◽  
David N. Potter ◽  
William A. Carlezon ◽  
...  

Author(s):  
Yuko Nakatake ◽  
Misa Yamada ◽  
Hiroki Furuie ◽  
Kazumi Yoshizawa ◽  
Mitsuhiko Yamada

Author(s):  
Kai Zhang ◽  
Akemi Sakamoto ◽  
Lijia Chang ◽  
Youge Qu ◽  
Siming Wang ◽  
...  

AbstractThe spleen is a large immune organ that plays a key role in the immune system. The precise molecular mechanisms underlying the relationship between the spleen and stress-related psychiatric disorders are unknown. Here we investigated the role of spleen in stress-related psychiatric disorders. FACS analysis was applied to determine the contribution of the spleen to susceptibility and resilience in mice that were subjected to chronic social defeat stress (CSDS). We found a notable increase in splenic volume and weight in CSDS-susceptible mice compared to control (no CSDS) mice and CSDS-resilient mice. The number of granulocytes, but not of T cells and B cells, in the spleen of susceptible mice was higher than in the spleen of both control and resilient mice. Interestingly, NKG2D (natural killer group 2, member D) expression in the spleen of CSDS-susceptible mice was higher than that in control mice and CSDS-resilient mice. In addition, NKG2D expression in the spleen of patients with depression was higher than that in controls. Both increased splenic weight and increased splenic NKG2D expression in CSDS-susceptible mice were ameliorated after a subsequent administration of (R)-ketamine. The present findings indicate a novel role of splenic NKG2D in stress susceptibility versus resilience in mice subjected to CSDS. Furthermore, abnormalities in splenic functions in CSDS-susceptible mice were ameliorated after subsequent injection of (R)-ketamine. Thus, the brain–spleen axis might, at least in part, contribute to the pathogenesis of stress-related psychiatric disorders such as depression.


Neuroreport ◽  
2020 ◽  
Vol 31 (9) ◽  
pp. 678-685
Author(s):  
Wenjuan Wang ◽  
Yong Qiao ◽  
Huiying Qu ◽  
Lin Zhu ◽  
Linlin Mu ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Hyun-Jung Park ◽  
Hyun-Soo Shim ◽  
Kyungeh An ◽  
Angela Starkweather ◽  
Kyung Soo Kim ◽  
...  

It has been known that activation of the central innate immune system or exposure to stress can disrupt balance of anti-/proinflammatory cytokines. The aim of the present study was to investigate the role of pro- and anti-inflammatory cytokines in the modulation of depressive-like behaviors, the hormonal and neurotransmitter systems in rats. We investigated whether centrally administered IL-1βis associated with activation of CNS inflammatory pathways and behavioral changes and whether treatment with IL-4 could modulate IL-1β-induced depressive-like behaviors and central neurotransmitter systems. Infusion of IL-4 significantly decreased IL-1β-induced anhedonic responses and increased social exploration and total activity. Treatment with IL-4 markedly blocked IL-1β-induced increase in PGE2and CORT levels. Also, IL-4 reduced IL-1β-induced 5-HT levels by inhibiting tryptophan hydroxylase (TPH) mRNA and activating serotonin transporter (SERT) in the hippocampus, and levels of NE were increased by activating tyrosine hydroxylase (TH) mRNA expression. These results demonstrate that IL-4 may locally contribute to the regulation of noradrenergic and serotonergic neurotransmission and may inhibit IL-1β-induced behavioral and immunological changes. The present results suggest that IL-4 modulates IL-1β-induced depressive behavior by inhibiting IL-1β-induced central glial activation and neurotransmitter alterations. IL-4 reduced central and systemic mediatory inflammatory activation, as well as reversing the IL-1β-induced alterations in neurotransmitter levels. The present findings contribute a biochemical pathway regulated by IL-4 that may have therapeutic utility for treatment of IL-1β-induced depressive behavior and neuroinflammation which warrants further study.


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