Brain-immune interactions in health and disease

Miyan, Jaleel

doi:10.3389/fnins.2014.00382

Cited by 8 publications

(10 citation statements)

References 18 publications

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“…The bidirectional interactions between the brain and immune system could take place in different organs or on various levels ( Denes and Miyan, 2014 ). There were several mechanisms by which peripheral proinflammatory cytokines such as IL-1β and TNF-α could affect the CNS and induce sickness response, including: 1) saturable transportation of cytokines into the brain, 2) leaking through cerebral endothelial or interacting with circumventricular organs lacking the blood-brain barrier, and 3) activation of afferent neurons of the vagus nerve ( Hosoi et al, 2002 ).…”

Section: Discussionmentioning

confidence: 99%

“…There were several mechanisms by which peripheral proinflammatory cytokines such as IL-1β and TNF-α could affect the CNS and induce sickness response, including: 1) saturable transportation of cytokines into the brain, 2) leaking through cerebral endothelial or interacting with circumventricular organs lacking the blood-brain barrier, and 3) activation of afferent neurons of the vagus nerve ( Hosoi et al, 2002 ). On the other hand, mood disorders, brain injuries, and stress were linked with development of systemic inflammatory conditions ( Denes and Miyan, 2014 ). Matsunaga et al (2013) suggested that the neural networks might regulate the secretion of peripheral proinflammatory cytokines.…”

Section: Discussionmentioning

confidence: 99%

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NLRP3 Inflammasome Mediates Chronic Mild Stress-Induced Depression in Mice via Neuroinflammation

Zhang

Liu

et al. 2015

International Journal of Neuropsychopharmacology

254

161

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Background:Evidence from both clinical and experimental research indicates that the immune-brain interaction plays a pivotal role in the pathophysiology of depression. A multi-protein complex of the innate immune system, the NLRP3 inflammasome regulates cleavage and secretion of proinflammatory cytokine interleukin-1β. The inflammasome detects various pathogen-associated molecule patterns and damage-associated molecule patterns, which then leads to a series of immune-inflammatory reactions.Methods:To explore the role of inflammasome activation in the underlying biological mechanisms of depression, we established a mouse model of depression with unpredictable chronic mild stress.Results:Mice subjected to chronic mild stress for 4 weeks had significantly higher serum corticosterone levels, serum interleukin-1β levels, and hippocampal active interleukin-1β protein levels. They also displayed depressive-like symptoms, including decreased sucrose preference and increased immobility time. Moreover, the hippocampi of chronic mild stress-exposed mice had significantly higher activity of caspase-1, which accompanied by higher protein levels of NLRP3 and the apoptotic speck-containing protein with a card. Pretreatment with the NLRP3 inflammasome inhibitor VX-765 decreased serum and hippocampal levels of interleukin-1β protein and significantly moderated the depressive-like behaviors induced by chronic mild stress.Conclusions:These data suggest the NLRP3 inflammasome mediates stress-induced depression via immune activation. Future procedures targeting the NLRP3 inflammasome may have promising effects in the prevention and treatment of depression.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

NLRP3 Inflammasome Mediates Chronic Mild Stress-Induced Depression in Mice via Neuroinflammation

Zhang

Liu

et al. 2015

International Journal of Neuropsychopharmacology

254

161

View full text Add to dashboard Cite

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“…We also suppose that GCLM gene downregulation and the probable subsequent diminished abundance of glutathione may underlie the development of autism as they may weaken the detoxification of xenobiotics that interfere with early postnatal neurodevelopment. 64 , 65 …”

Section: Discussionmentioning

confidence: 99%

Expression of Reactive Oxygen Species–Related Transcripts in Egyptian Children With Autism

et al. 2017

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The molecular basis of the pathophysiological role of oxidative stress in autism is understudied. Herein, we used polymerase chain reaction (PCR) array to analyze transcriptional pattern of 84 oxidative stress genes in peripheral blood mononuclear cell pools isolated from 32 autistic patients (16 mild/moderate and 16 severe) and 16 healthy subjects (each sample is a pool from 4 autistic patients or 4 controls). The PCR array data were further validated by quantitative real-time PCR in 80 autistic children (55 mild/moderate and 25 severe) and 60 healthy subjects. Our data revealed downregulation in GCLM, SOD2, NCF2, PRNP, and PTGS2 transcripts (1.5, 3.8, 1.2, 1.7, and 2.2, respectively;P < .05 for all) in autistic group compared with controls. In addition, TXN and FTH1 exhibited 1.4- and 1.7-fold downregulation, respectively, in severe autistic patients when compared with mild/moderate group (P = .005 and .0008, respectively). This study helps in a better understanding of the underlying biology and related genetic factors of autism, and most importantly, it presents suggested candidate biomarkers for diagnosis and prognosis purposes as well as targets for therapeutic intervention.

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“…It has been proposed that damage to brain tissue after a TBI may initiate local metabolic and inflammatory processes, resulting in the release of a number of inflammatory mediators and damage-associated molecular pattern (DAMP) molecules ( 7 , 8 ). These molecules then cross a dysfunctional blood brain barrier (BBB) and enter the circulation to recruit peripheral immune cells to the brain, initiating bidirectional communication between the CNS and the systemic immune system ( 8 – 10 ). Thus, peripheral blood samples may contain molecules derived from the CNS and/or the periphery as a secondary response to injury.…”

Section: Introductionmentioning

confidence: 99%

Blood Biomarkers in Moderate-To-Severe Traumatic Brain Injury: Potential Utility of a Multi-Marker Approach in Characterizing Outcome

et al. 2015

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BackgroundBlood biomarkers are valuable tools for elucidating complex cellular and molecular mechanisms underlying traumatic brain injury (TBI). Profiling distinct classes of biomarkers could aid in the identification and characterization of initial injury and secondary pathological processes. This study characterized the prognostic performance of a recently developed multi-marker panel of circulating biomarkers that reflect specific pathogenic mechanisms including neuroinflammation, oxidative damage, and neuroregeneration, in moderate-to-severe TBI patients.Materials and methodsPeripheral blood was drawn from 85 isolated TBI patients (n = 60 severe, n = 25 moderate) at hospital admission, 6-, 12-, and 24-h post-injury. Mortality and neurological outcome were assessed using the extended Glasgow Outcome Scale. A multiplex platform was designed on MULTI-SPOT® plates to simultaneously analyze human plasma levels of s100 calcium binding protein beta (s100B), glial fibrillary acidic protein (GFAP), neuron specific enolase (NSE), brain-derived neurotrophic factor (BDNF), monocyte chemoattractant protein (MCP)-1, intercellular adhesion molecule (ICAM)-5, and peroxiredoxin (PRDX)-6. Multivariable logistic regression and area under the receiver-operating characteristic curve (AUC) were used to evaluate both individual and combined predictive abilities of these markers for 6-month neurological outcome and mortality after TBI.ResultsUnfavorable neurological outcome was associated with elevations in s100B, GFAP, and MCP-1. Mortality was related to differences in six of the seven markers analyzed. Combined admission concentrations of s100B, GFAP, and MCP-1 were able to discriminate favorable versus unfavorable outcome (AUC = 0.83), and survival versus death (AUC = 0.87), although not significantly better than s100B alone (AUC = 0.82 and 0.86, respectively).ConclusionThe multi-marker panel of TBI-related biomarkers performed well in discriminating unfavorable and favorable outcomes in the acute period after moderate-to-severe TBI. However, the combination of these biomarkers did not outperform s100B alone.

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Brain-immune interactions in health and disease

Cited by 8 publications

References 18 publications

NLRP3 Inflammasome Mediates Chronic Mild Stress-Induced Depression in Mice via Neuroinflammation

NLRP3 Inflammasome Mediates Chronic Mild Stress-Induced Depression in Mice via Neuroinflammation

Expression of Reactive Oxygen Species–Related Transcripts in Egyptian Children With Autism

Blood Biomarkers in Moderate-To-Severe Traumatic Brain Injury: Potential Utility of a Multi-Marker Approach in Characterizing Outcome

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