Glucocorticoids mediate stress-induced priming of microglial pro-inflammatory responses. - Wikidata - awgldk - TriplyDB

Glucocorticoids mediate stress-induced priming of microglial pro-inflammatory responses.

Glucocorticoids mediate stress-induced priming of microglial pro-inflammatory responses.

http://www.wikidata.org/entity/Q42381161

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The Pro-inflammatory Effects of Glucocorticoids in the Brain Chronic Stress and Glucocorticoids: From Neuronal Plasticity to Neurodegeneration Microglial Cells as a Link between Cannabinoids and the Immune Hypothesis of Psychiatric Disorders Role of Glia in Stress-Induced Enhancement and Impairment of Memory Surveillance, phagocytosis, and inflammation: how never-resting microglia influence adult hippocampal neurogenesis Stress sounds the alarmin: The role of the danger-associated molecular pattern HMGB1 in stress-induced neuroinflammatory priming Acute and chronic stress-induced disturbances of microglial plasticity, phenotype and function The microbiome: A key regulator of stress and neuroinflammation Stress-induced neuroinflammatory priming: A liability factor in the etiology of psychiatric disorders Neuron-Microglia Interactions in Mental Health Disorders: "For Better, and For Worse"The permissive role of glucocorticoids in neuroinflammatory priming: mechanisms and insights Chronic exposure to exogenous glucocorticoids primes microglia to pro-inflammatory stimuli and induces NLRP3 mRNA in the hippocampus Inflammation and the neural diathesis-stress hypothesis of schizophrenia: a reconceptualization Stress-induced neuroinflammatory priming is time of day dependent.Broken or maladaptive? Altered trajectories in neuroinflammation and behavior after early life adversity Inflammation and the two-hit hypothesis of schizophrenia.Missing and Possible Link between Neuroendocrine Factors, Neuropsychiatric Disorders, and Microglia Potent and multiple regulatory actions of microglial glucocorticoid receptors during CNS inflammation.Chronic glucocorticoid exposure activates BK-NLRP1 signal involving in hippocampal neuron damage.Toll-like receptor 4: innate immune regulator of neuroimmune and neuroendocrine interactions in stress and major depressive disorder At the extreme end of the psychoneuroimmunological spectrum: delirium as a maladaptive sickness behaviour response.Select steroid hormone glucuronide metabolites can cause toll-like receptor 4 activation and enhanced pain Monocyte trafficking to the brain with stress and inflammation: a novel axis of immune-to-brain communication that influences mood and behavior Changes of cytokines during a spaceflight analog--a 45-day head-down bed rest.Microglia inflammatory responses are controlled by an intrinsic circadian clock.Differential glucocorticoid metabolism in patients with persistent versus resolving inflammatory arthritis.A pre-conditioning stress accelerates increases in mouse plasma inflammatory cytokines induced by stress The importance of biological oscillators for hypothalamic-pituitary-adrenal activity and tissue glucocorticoid response: coordinating stress and neurobehavioural adaptation.The evolving landscape of neurotoxicity by unconjugated bilirubin: role of glial cells and inflammation.Models and mechanisms for hippocampal dysfunction in obesity and diabetes Pigment Epithelium-Derived Factor (PEDF) mediates cartilage matrix loss in an age-dependent manner under inflammatory conditions.Effects of histamine H1 receptor signaling on glucocorticoid receptor activity. Role of canonical and non-canonical pathways Prior exposure to repeated morphine potentiates mechanical allodynia induced by peripheral inflammation and neuropathy.Testing the nanoparticle-allostatic cross-adaptation-sensitization model for homeopathic remedy effects The redox state of the alarmin HMGB1 is a pivotal factor in neuroinflammatory and microglial priming: A role for the NLRP3 inflammasome.Neuroinflammation, neuroautoimmunity, and the co-morbidities of complex regional pain syndrome.Possible involvement of TLRs and hemichannels in stress-induced CNS dysfunction via mastocytes, and glia activation.Programmed symptoms: disparate effects united by purpose.Glucocorticoids Mediate Short-Term High-Fat Diet Induction of Neuroinflammatory Priming, the NLRP3 Inflammasome, and the Danger Signal HMGB1 Blocking toll-like receptor 2 and 4 signaling during a stressor prevents stress-induced priming of neuroinflammatory responses to a subsequent immune challenge.

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P2860

Glucocorticoids mediate stress-induced priming of microglial pro-inflammatory responses.

http://www.wikidata.org/entity/Q42381161

description

2011 nî lūn-bûn

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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2011年论文

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2011年论文

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name

Glucocorticoids mediate stress-induced priming of microglial pro-inflammatory responses.

@en

Glucocorticoids mediate stress-induced priming of microglial pro-inflammatory responses.

@nl

type

label

Glucocorticoids mediate stress-induced priming of microglial pro-inflammatory responses.

@en

Glucocorticoids mediate stress-induced priming of microglial pro-inflammatory responses.

@nl

prefLabel

Glucocorticoids mediate stress-induced priming of microglial pro-inflammatory responses.

@en

Glucocorticoids mediate stress-induced priming of microglial pro-inflammatory responses.

@nl

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J.BBI.2011.10.005

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Brain, Behavior, and Immunity

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Glucocorticoids mediate stress-induced priming of microglial pro-inflammatory responses.

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P2093

Brittany M Thompson

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Matthew G Frank

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Steven F Maier

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P2860

Gapped BLAST and PSI-BLAST: a new generation of protein database search programs

The role of pattern-recognition receptors in innate immunity: update on Toll-like receptors

11beta-Hydroxysteroid dehydrogenase in the brain: a novel regulator of glucocorticoid action?

Gene expression changes in the hypothalamus provide evidence for regionally-selective changes in IL-1 and microglial markers after acute stress

Noradrenaline induces IL-1ra and IL-1 type II receptor expression in primary glial cells and protects against IL-1beta-induced neurotoxicity

Social stress enhances IL-1beta and TNF-alpha production by Porphyromonas gingivalis lipopolysaccharide-stimulated CD11b+ cells.

Cross-sensitization between immune and non-immune stressors. A role in the etiology of depression?

Social stress induces glucocorticoid resistance in macrophages.

Cellular processing of the glucocorticoid receptor gene and protein: new mechanisms for generating tissue-specific actions of glucocorticoids.

Mifepristone: bioavailability, pharmacokinetics and use-effectiveness.

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