The reciprocal interaction of sympathetic nervous system and cAMP-PKA-NF-kB pathway in immune suppression after experimental stroke

Zuo, Lei; Shi, Luhang; Yan, Fuling

doi:10.1016/j.neulet.2016.05.066

Cited by 43 publications

(35 citation statements)

References 30 publications

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“…Compared with 24 and 48 h after pMCAO, the motor function of rats shows slight recovery at 72 h in rotarod test [32]. The levels of transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) and of heme oxygenase-1 (HO-1) peak at 24 h and decrease at 72 h after ischemia, and NF-jB is also down-regulated at 72 h [33,34]. In addition, the serum level of the proinflammatory factor TNF-a is decreased, while that of the anti-inflammatory cytokine IL-10 is increased at 72 h after ischemia [34].…”

Section: Discussionmentioning

confidence: 99%

“…The levels of transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) and of heme oxygenase-1 (HO-1) peak at 24 h and decrease at 72 h after ischemia, and NF-jB is also down-regulated at 72 h [33,34]. In addition, the serum level of the proinflammatory factor TNF-a is decreased, while that of the anti-inflammatory cytokine IL-10 is increased at 72 h after ischemia [34]. Therefore, we speculate that transcription factors regulate the levels of aquaporins, TJ proteins and inflammatory cytokines, further inducing a recovery of BBB integrity.…”

Section: Discussionmentioning

confidence: 99%

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Time-course investigation of blood–brain barrier permeability and tight junction protein changes in a rat model of permanent focal ischemia

et al. 2017

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Permanent middle cerebral artery occlusion (pMCAO) is an animal model that is widely used to simulate human ischemic stroke. However, the timing of the changes in the expression of tight junction (TJ) proteins and synaptic proteins associated with pMCAO remain incompletely understood. Therefore, to further explore the characteristics and mechanisms of blood-brain barrier (BBB) damage during cerebral ischemic stroke, we used a pMCAO rat model to define dynamic changes in BBB permeability within 120 h after ischemia in order to examine the expression levels of the TJ proteins claudin-5 and occludin and the synaptic proteins synaptophysin (SYP) and postsynaptic density protein 95 (PSD95). In our study, Evans blue content began to increase at 4 h and was highest at 8 and 120 h after ischemia. TTC staining showed that cerebral infarction was observed at 4 h and that the percentage of infarct volume increased with time after ischemia. The expression levels of claudin-5 and occludin began to decline at 1 h and were lowest at 8 and 120 h after ischemia. The expression levels of SYP and PSD95 decreased from 12 to 120 h after ischemia. GFAP, an astrocyte marker, gradually increased in the cortex penumbra over time post-ischemia. Our study helps clarify the characteristics of pMCAO models and provides evidence supporting the translational potential of animal stroke models.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Time-course investigation of blood–brain barrier permeability and tight junction protein changes in a rat model of permanent focal ischemia

et al. 2017

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“…The inflammatory response is also modulated by the autonomic nervous system, physiological activation of sympathetic nervous system is in general pro‐inflammatory, while parasympathetic activity is antiinflammatory (Pongratz & Straub, ; Tracey, ). However, severe conditions, such as stroke or polytrauma may be associated with delayed immunosuppression, possibly due to fact that severe conditions represent very strong stress, which may be associated with overstimulation of sympathetic nervous system and subsequent direct or rebound immunodepression (Jiang, ; Yan & Zhang, ; Zuo, Shi, & Yan, ).…”

Section: Strokementioning

confidence: 99%

Evolutionary concept of inflammatory response and stroke

Ďuriš

Jurajda

2019

J of Neuroscience Research

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The immune system plays an important role under both physiological and pathological conditions. Immune surveillance as well as defense and healing processes are crucial for the organism, but the immune system has a natural tendency to act aggressively when excessively stimulated. We may assume that the immune system is not designed to deal with severe conditions, such as polytrauma or severe stroke, because these are not compatible with life in the wilderness and evolution has no chance to act in such cases. These conditions are associated with exaggerated/deregulated inflammatory response, which may cause more damage than initial pathology. In this article, we would like to sketch a basic concept of the immune system-brain interactions from the evolutionary point of view and to discuss some implications related to stroke. K E Y W O R D S evolution, inflammation, stroke | 99 DURIS anD JURaJDa

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“…Cyclic AMP in turn represents the second messengers of many G-protein mediated hormone and cytokine responses [154] (e.g., induction of hepatic glycogenolysis after β-adrenergic stimulation [155]), processes of cell differentiation, cytoskeletal remodeling and proliferation in addition to apoptosis and immune modulation [156]. While AGE formation is thought to be part of pro-inflammatory signaling cascades (via RAGE and NFκB), recent in vivo studies suggest that globally high cAMP concentrations have moderate immunosuppressive effects [157,158]. Furthermore, cAMP-impaired neutrophil chemotaxis in vitro [159] decreased the release of histamine and leukotrienes from basophils or mast cells [160], which significantly reduced ROS formation [161,162].…”

Section: Different Aspects Of the Stress Response In Sepsismentioning

confidence: 99%

The Glyoxalase System and Methylglyoxal-Derived Carbonyl Stress in Sepsis: Glycotoxic Aspects of Sepsis Pathophysiology

Schmoch

Uhle

Siegler

et al. 2017

IJMS

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Sepsis remains one of the leading causes of death in intensive care units. Although sepsis is caused by a viral, fungal or bacterial infection, it is the dysregulated generalized host response that ultimately leads to severe dysfunction of multiple organs and death. The concomitant profound metabolic changes are characterized by hyperglycemia, insulin resistance, and profound transformations of the intracellular energy supply in both peripheral and immune cells. A further hallmark of the early phases of sepsis is a massive formation of reactive oxygen (ROS; e.g., superoxide) as well as nitrogen (RNS; e.g., nitric oxide) species. Reactive carbonyl species (RCS) form a third crucial group of highly reactive metabolites, which until today have been not the focus of interest in sepsis. However, we previously showed in a prospective observational clinical trial that patients suffering from septic shock are characterized by significant methylglyoxal (MG)-derived carbonyl stress, with the glyoxalase system being downregulated in peripheral blood mononuclear cells. In this review, we give a detailed insight into the current state of research regarding the metabolic changes that entail an increased MG-production in septicemia. Thus, we point out the special role of the glyoxalase system in the context of sepsis.

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The reciprocal interaction of sympathetic nervous system and cAMP-PKA-NF-kB pathway in immune suppression after experimental stroke

Cited by 43 publications

References 30 publications

Time-course investigation of blood–brain barrier permeability and tight junction protein changes in a rat model of permanent focal ischemia

Time-course investigation of blood–brain barrier permeability and tight junction protein changes in a rat model of permanent focal ischemia

Evolutionary concept of inflammatory response and stroke

The Glyoxalase System and Methylglyoxal-Derived Carbonyl Stress in Sepsis: Glycotoxic Aspects of Sepsis Pathophysiology

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