Neuron‐glial cell communication in the traumatic stress‐induced immunomodulation

Zhao, Hui; Xiao, Shifu; Kong, Xiaoyan; Wang, Jun; Cao, Xiao-Ding; Loh, Horace H.; Law, Ping Yee

doi:10.1002/syn.20861

Cited by 8 publications

(6 citation statements)

References 41 publications

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“…Ultimately, reductions in synaptic numbers and the amplitude of the field excitatory postsynaptic potential (EPSP) happened during the aging [31]. In the present study, we demonstrated that synaptic Fyn activity was greatly augmented at day 3after trauma, with higher magnitude in 1-year mice that that in 2-month counterpart, together with our previous observation, namely, discordant Fyn signaling events was responsible for the deteriorated immuno-suppression and prolonged recovery aged rats during the traumatic stress [8,32], then, the result reinforced the idea that Fyn signaling might actively communicate with pre and post-synaptic elements of neuronal terminals influencing stress like events.…”

Section: Discussionsupporting

confidence: 72%

Age-Dependent Neuroimmune Modulation of IGF-1R in the Traumatic Mice

Zhao

Cao

2012

Immun Ageing

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BackgroundAge-dependent neuroimmune modulation following traumatic stress is accompanied by discordant upregulation of Fyn signaling in the frontal cortex, but the mechanistic details of the potential cellular behavior regarding IGF-1R/Fyn have not been established.MethodsTrans-synaptic IGF-1R signaling during the traumatic stress was comparably examined in wild type, Fyn (−/−) and MOR (−/−) mice. Techniques included primary neuron culture, in vitro kinase activity, immunoprecipitation, Western Blot, sucrose discontinuous centrifugation. Besides that, [3 H] incorporation was used to assay lymphocyte proliferation and NK cell activity.ResultsWe demonstrate robust upregulation of synaptic Fyn activity following traumatic stress, with higher amplitude in 2-month mice than that in 1-year counterpart. We also established that the increased Fyn signaling is accompanied by its molecular connection with IGF-1R within the synaptic zone. Detained analysis using Fyn (−/−) and MOR (−/−) mice reveal that IGF-1R/Fyn signaling is governed to a large extent by mu opioid receptor (MOR), and with age-dependent manner; these signaling cascades played a central role in the modulation of lymphocyte proliferation and NK cell activity.ConclusionsOur data argued for a pivotal role of synaptic IGF-1R/Fyn signaling controlled by MOR downstream signaling cascades were crucial for the age-dependent neuroimmune modulation following traumatic stress. The result here might present a new quality of synaptic cellular communication governing the stress like events and have significant potential for the development of therapeutic approaches designed to minimize the heightened vulnerability during aging.

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Section: Discussionsupporting

confidence: 72%

Age-Dependent Neuroimmune Modulation of IGF-1R in the Traumatic Mice

Zhao

Cao

2012

Immun Ageing

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“…Microglia are directly activated when exposed to B. burgdorferi and involved in neuronal-glia and glial communication [32]. While multiple cell types in the brain express MHC, in studies using minocycline (a suppressor of microglia) microglia activation was essential to induce stress-induced ERK1/2 neuroimmune modulation [33]. Further, the rapid increase in the expression of IL-1 receptor on microglia in response to endotoxin and vascular occlusion support the role of microglia as being a primary initiator of the neuroimmune response [34,35].…”

Section: Discussionmentioning

confidence: 99%

Acetate supplementation reduces microglia activation and brain interleukin-1β levels in a rat model of Lyme neuroborreliosis

Brissette

Houdek

Floden

et al. 2012

J Neuroinflammation

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BackgroundWe have found that acetate supplementation significantly reduces neuroglia activation and pro-inflammatory cytokine release in a rat model of neuroinflammation induced with lipopolysaccharide. To test if the anti-inflammatory effect of acetate supplementation is specific to a TLR4-mediated injury, we measured markers of neuroglia activation in rats subjected to B. burgdorferi-induced neuroborreliosis that is mediated in large part by a TLR2-type mechanism.MethodsIn this study, rats were subjected to Lyme neuroborreliosis following an intravenous infusion of B. burgdorferi (B31-MI-16). Acetate supplementation was induced using glyceryl triacetate (6g/kg) by oral gavage. Immunohistochemistry, qPCR, and western blot analyses were used to measure bacterial invasion into the brain, neuroglial activation, and brain and circulating levels of interleukin 1β. Statistical analysis was performed using one-way analysis of variance (ANOVA) followed by a Tukey’s post hoc tests or using a Student’s t test assuming unequal variances when appropriate.ResultsWe found that acetate supplementation significantly reduced microglia activation by 2-fold as determined by immunohistochemical and western blot analysis. Further, acetate supplementation also reduced the expression of the pro-inflammatory cytokine IL-1β by 2-fold as compared to controls. On the other hand, the inoculation of rats with B. burgdorferi had no effect on astroglial activation as determined by immunocytochemistry and western blot analysis despite significant increases in circulation levels of antigen toward B. burgdorferi and presence of the bacteria in the central nervous system.ConclusionsThese results suggest that microglial activation is an essential component to neuroborreliosis and that acetate supplementation may be an effective treatment to reduce injury phenotype and possibly injury progression in Lyme neuroborreliosis.

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“…RSK2 is as well implicated in cellular functions (10,11,15,23,36,52) and tumorigenesis (12,33). Although RSK is known to be regulated at the posttranscriptional level by phosphorylation (12,36), it has also been shown that the expression of RSK protein in the frontal cortex is enhanced by hypoxic preconditioning (44) or traumatic stress (54). In this work, we found that daily stress exposure induced dorsal horn RSK2 expression in the dorsal horn of rats.…”

Section: Discussionmentioning

confidence: 54%

Glucocorticoid mediates water avoidance stress-sensitized colon-bladder cross-talk via RSK2/PSD-95/NR2B in rats

Peng

Hsieh

Lai

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

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Unexpected environmental and social stimuli could trigger stress. Although coping with stress is essential for survival, long-term stress impacts visceral functions, and therefore, it plays a role in the development and exacerbation of symptoms of gastrointestinal/urogenital disorders. The aim of this study is to characterize the role of corticosterone in stress-sensitized colon-bladder cross-talk, a phenomenon presumed to underlie the comorbidity of functional bowel and bladder disorders. Cystometry and protein/mRNA expression in the lumbosacral dorsal horn (L6-S1) in response to intracolonic mustard oil (MO) instillation were analyzed in female Wistar-Kyoto rats subjected to water avoidance stress (WAS; 1 h/day for 10 days) or sham stress (WAsham). Whereas it had no effect on baseline-voiding function, chronic stress upregulated plasma corticosterone concentration and dorsal horn spinal p90 ribosomal S6 kinase 2 (RSK2) protein/mRNA levels, and RSK2 immunoreactivity colocalized with NeuN-positive neurons. Intracolonic MO dose-dependently decreased intrercontraction intervals and threshold pressure, provoked spinal RSK2 and NR2B phosphorylation, and enhanced PSD-95-RSK2 and PSD-95-NR2B coupling. Intrathecal kaempferol (a RSK2 activation antagonist; 30 min before MO instillation), bilateral adrenalectomy (7 days prior the stress paradigm), and subcutaneous RU-38486 (a glucocorticoid receptor antagonist; 30 min daily before stress sessions), but not RU-28318 (a mineralocorticoid receptor antagonist), attenuated MO-induced bladder hyperactivity, protein phosphorylation, and protein-protein interactions in the WAS group. Our results suggest that stress-associated glucocorticoid release mediates WAS-dependent sensitization of colon-bladder cross-talk via the spinal RSK2/PSD-95/NR2B cascade and offer a possibility for developing pharmacological strategies for the treatment of stress-related pelvic pain.

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Neuron‐glial cell communication in the traumatic stress‐induced immunomodulation

Cited by 8 publications

References 41 publications

Age-Dependent Neuroimmune Modulation of IGF-1R in the Traumatic Mice

Age-Dependent Neuroimmune Modulation of IGF-1R in the Traumatic Mice

Acetate supplementation reduces microglia activation and brain interleukin-1β levels in a rat model of Lyme neuroborreliosis

Glucocorticoid mediates water avoidance stress-sensitized colon-bladder cross-talk via RSK2/PSD-95/NR2B in rats

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