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Inflammasome brain

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https://www.readbyqxmd.com/read/28202418/ros-txnip-pathway-contributes-to-thrombin-induced-nlrp3-inflammasome-activation-and-cell-apoptosis-in-bv2-cells
#1
Dandan Zuo, Xinchun Ye, Lu Yu, Liang Zhang, Jiao Tang, Chengcheng Cui, Lei Bao, Kun Zan, Zuohui Zhang, Xinxin Yang, Hao Chen, Hai Tang, Jie Zu, Hongjuan Shi, Guiyun Cui
There is no effective therapy for intracerebral hemorrhage (ICH) because of poor understanding of the mechanisms of brain injury after hemorrhage. The NLRP3 inflammasome, as a vital component of innate immune system, which is associated with a wide range of human CNS disorders, including ICH. But its detailed mechanisms in ICH remain mainly unclear. In this study, BV2 cells with thrombin exposure were used to investigate the role of NLRP3 inflammasome in thrombin-induced brain injury. We used western blot to detect NLRP3 inflammasome activation and the expression of thioredoxin binding protein (TXNIP), DCFH-DA to investigate intracellular reactive oxygen species (ROS), flow cytometry to analyze apoptosis...
February 12, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28186177/the-far-reaching-scope-of-neuroinflammation-after-traumatic-brain-injury
#2
REVIEW
Dennis W Simon, Mandy J McGeachy, Hülya Bayır, Robert S B Clark, David J Loane, Patrick M Kochanek
The 'silent epidemic' of traumatic brain injury (TBI) has been placed in the spotlight as a result of clinical investigations and popular press coverage of athletes and veterans with single or repetitive head injuries. Neuroinflammation can cause acute secondary injury after TBI, and has been linked to chronic neurodegenerative diseases; however, anti-inflammatory agents have failed to improve TBI outcomes in clinical trials. In this Review, we therefore propose a new framework of targeted immunomodulation after TBI for future exploration...
February 10, 2017: Nature Reviews. Neurology
https://www.readbyqxmd.com/read/28181102/cerebrospinal-fluid-nlrp3-is-increased-after-severe-traumatic-brain-injury-in-infants-and-children
#3
Jessica S Wallisch, Dennis W Simon, Hülya Bayır, Michael J Bell, Patrick M Kochanek, Robert S B Clark
BACKGROUND: Inflammasome-mediated neuroinflammation may cause secondary injury following traumatic brain injury (TBI) in children. The pattern recognition receptors NACHT domain-, Leucine-rich repeat-, and PYD-containing Protein 1 (NLRP1) and NLRP3 are essential components of their respective inflammasome complexes. We sought to investigate whether NLRP1 and/or NLRP3 abundance is altered in children with severe TBI. METHODS: Cerebrospinal fluid (CSF) from children (n = 34) with severe TBI (Glasgow coma scale score [GCS] ≤8) who had externalized ventricular drains (EVD) placed for routine care was evaluated for NLRP1 and NLRP3 at 0-24, 25-48, 49-72, and >72 h post-TBI and was compared to infection-free controls that underwent lumbar puncture to rule out CNS infection (n = 8)...
February 8, 2017: Neurocritical Care
https://www.readbyqxmd.com/read/28178176/nlrp12-inflammasome-expression-in-the-rat-brain-in-response-to-lps-during-morphine-tolerance
#4
Sulie L Chang, Wenfei Huang, Xin Mao, Sabroni Sarkar
Morphine, an effective but addictive analgesic, can profoundly affect the inflammatory response to pathogens, and long-term use can result in morphine tolerance. Inflammasomes are protein complexes involved in the inflammatory response. The nucleotide-binding oligomerization domain-like receptor (NLR) Family Pyrin Domain Containing (NLRP) 12 (NLRP12) inflammasome has been reported to have anti-inflammatory activity. In this study, we examined the expression of NLRP12 inflammasome related genes in the adult F344 rat brain in response to the bacterial endotoxin lipopolysaccharide (LPS) in the presence and absence of morphine tolerance...
February 6, 2017: Brain Sciences
https://www.readbyqxmd.com/read/28164443/low-level-light-emitting-diode-led-therapy-suppresses-inflammasome-mediated-brain-damage-in-experimental-ischemic-stroke
#5
Hae In Lee, Sae-Won Lee, Nam Gyun Kim, Kyoung-Jun Park, Byung Tae Choi, Yong-Il Shin, Hwa Kyoung Shin
Use of photostimulation including low-level light emitting diode (LED) therapy has broadened greatly in recent years because it is compact, portable, and easy to use. Here, the effects of photostimulation by LED (610 nm) therapy on ischemic brain damage was investigated in mice in which treatment started after a stroke in a clinically relevant setting. The mice underwent LED therapy (20 min) twice a day for 3 days, commencing at 4 hours post-ischemia. LED therapy group generated a significantly smaller infarct size and improvements in neurological function based on neurologic test score...
February 6, 2017: Journal of Biophotonics
https://www.readbyqxmd.com/read/28153732/zika-virus-induces-inflammasome-activation-in-the-glial-cell-line-u87-mg
#6
Paola Maura Tricarico, Ilaria Caracciolo, Sergio Crovella, Pierlanfranco D'Agaro
In the last years, neurological complications related to Zika virus (ZIKV) infection have emerged as an important threat to public health worldwide. ZIKV infection has been associated to neurological disorders such as congenital microcephaly in newborns and Guillain-Barré syndrome, myelopathy and encephalitis in adults. ZIKV is characterized by neurotropism and neurovirulence. Several studies have identified microglial nodules, gliosis, neuronal and glial cells degeneration and necrosis in the brain of ZIKV infected infants, suggesting that ZIKV could play a role in these neurological disorders through neuroinflammation and microglial activation...
January 30, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28132925/combined-nadph-and-the-nox-inhibitor-apocynin-provides-greater-anti-inflammatory-and-neuroprotective-effects-in-a-mouse-model-of-stroke
#7
Yuan-Yuan Qin, Mei Li, Xing Feng, Jian Wang, Lijuan Cao, Xi-Kui Shen, Jieyu Chen, Meiling Sun, Rui Sheng, Feng Han, Zheng-Hong Qin
Our previous study has reported that the pentose phosphate pathway product nicotinamide adenine dinucleotide phosphate (NADPH) protected neurons against ischemia/reperfusion-induced brain injury. NADPH can either act as a co-enzyme to produce GSH or a substrate of NADPH oxidase (NOX) to generate ROS. This study was designed to elucidate the effects of co-treatment with NADPH and NOX inhibitor apocynin on ischemia/reperfusion-induced brain inflammation and neuronal injury. The results showed that both NADPH and apocynin markedly attenuated ischemia/reperfusion-induced increases in the levels of NOX2, NOX4 and ROS...
January 26, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28129888/alzheimer-s-disease-innate-immunity-gone-awry
#8
Theodore B VanItallie
Inflammation is an immune activity designed to protect the host from pathogens and noxious agents. In its low-intensity form, presence of an inflammatory process must be inferred from appropriate biomarkers. Occult neuroinflammation is not just secondary to Alzheimer's disease (AD) but may contribute to its pathogenesis and promote its progression. A leaky blood-brain barrier (BBB) has been observed in early AD and may play a role in its initiation and development. Studies of the temporal evolution of AD's biomarkers have shown that, in AD, the brain's amyloid burden correlates poorly with cognitive decline...
January 11, 2017: Metabolism: Clinical and Experimental
https://www.readbyqxmd.com/read/28129542/pathogen-mediated-inhibition-of-anorexia-promotes-host-survival-and-transmission
#9
Sheila Rao, Alexandria M Palaferri Schieber, Carolyn P O'Connor, Mathias Leblanc, Daniela Michel, Janelle S Ayres
Sickness-induced anorexia is a conserved behavior induced during infections. Here, we report that an intestinal pathogen, Salmonella Typhimurium, inhibits anorexia by manipulating the gut-brain axis. Inhibition of inflammasome activation by the S. Typhimurium effector, SlrP, prevented anorexia caused by IL-1β-mediated signaling to the hypothalamus via the vagus nerve. Rather than compromising host defenses, pathogen-mediated inhibition of anorexia increased host survival. SlrP-mediated inhibition of anorexia prevented invasion and systemic infection by wild-type S...
January 26, 2017: Cell
https://www.readbyqxmd.com/read/28117838/early-onset-of-inflammation-during-ontogeny-of-bipolar-disorder-the-nlrp2-inflammasome-gene-distinctly-differentiates-between-patients-and-healthy-controls-in-the-transition-between-ips-cell-and-neural-stem-cell-stages
#10
D Vizlin-Hodzic, Q Zhai, S Illes, K Södersten, K Truvé, T Z Parris, P K Sobhan, S Salmela, S T Kosalai, C Kanduri, J Strandberg, H Seth, T O Bontell, E Hanse, H Ågren, K Funa
Neuro-inflammation and neuronal communication are considered as mis-regulated processes in the aetiology and pathology of bipolar disorder (BD). Which and when specific signal pathways become abnormal during the ontogeny of bipolar disorder patients is unknown. To address this question, we applied induced pluripotent stem cell (iPSC) technology followed by cortical neural differentiation on adipocyte-derived cells from BD type I patients (with psychotic episodes in psychiatric history) and healthy volunteers (controls)...
January 24, 2017: Translational Psychiatry
https://www.readbyqxmd.com/read/28109896/the-nlrp3-inflammasome-modulates-sleep-and-nrem-sleep-delta-power-induced-by-spontaneous-wakefulness-sleep-deprivation-and-lipopolysaccharide
#11
Mark R Zielinski, Dmitry Gerashchenko, Svetlana A Karpova, Varun Konanki, Robert W McCarley, Fayyaz S Sutterwala, Robert E Strecker, Radhika Basheer
Both sleep loss and pathogens can enhance brain inflammation, sleep, and sleep intensity as indicated by electroencephalogram delta (δ) power. The pro-inflammatory cytokine interleukin-1 beta (IL-1β) is increased in the cortex after sleep deprivation (SD) and in response to the Gram-negative bacterial cell-wall component lipopolysaccharide (LPS), although the exact mechanisms governing these effects are unknown. The nucleotide-binding domain and leucine-rich repeat protein-3 (NLRP3) inflammasome protein complex forms in response to changes in the local environment and, in turn, activates caspase-1 to convert IL-1β into its active form...
January 18, 2017: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/28092085/evidence-that-nf-%C3%AE%C2%BAb-and-mapk-signaling-promotes-nlrp-inflammasome-activation-in-neurons-following-ischemic-stroke
#12
David Yang-Wei Fann, Yun-An Lim, Yi-Lin Cheng, Ker-Zhing Lok, Prasad Chunduri, Sang-Ha Baik, Grant R Drummond, S Thameem Dheen, Christopher G Sobey, Dong-Gyu Jo, Christopher Li-Hsian Chen, Thiruma V Arumugam
Multi-protein complexes, termed "inflammasomes," are known to contribute to neuronal cell death and brain injury following ischemic stroke. Ischemic stroke increases the expression and activation of nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) Pyrin domain containing 1 and 3 (NLRP1 and NLRP3) inflammasome proteins and both interleukin (IL)-1β and IL-18 in neurons. In this study, we provide evidence that activation of either the NF-κB and MAPK signaling pathways was partly responsible for inducing the expression and activation of NLRP1 and NLRP3 inflammasome proteins and that these effects can be attenuated using pharmacological inhibitors of these two pathways in neurons and brain tissue under in vitro and in vivo ischemic conditions, respectively...
January 14, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28077335/omega-3-fatty-acids-regulate-nlrp3-inflammasome-activation-and-prevent-behavior-deficits-after-traumatic-brain-injury
#13
Chao Lin, Honglu Chao, Zheng Li, Xiupeng Xu, Yinlong Liu, Zhongyuan Bao, Lijun Hou, Yan Liu, Xiaoming Wang, Yongping You, Ning Liu, Jing Ji
Omega-3 fatty acids (ω-3 FAs) attenuate inflammation and improve neurological outcome in response to traumatic brain injury (TBI), but the specific anti-inflammatory mechanisms remain to be elucidated. Here we found that NLRP3 inflammasome and subsequent pro-inflammatory cytokines were activated in human brains after TBI. Rats treated with ω-3 FAs had significantly less TBI-induced caspase-1 cleavage and IL-1β secretion than those with vehicle. G protein-coupled receptor 40 (GPR40) was observed to be involved in this anti-inflammation...
January 8, 2017: Experimental Neurology
https://www.readbyqxmd.com/read/28058465/fish-oil-supplementation-attenuates-neuroinflammation-and-alleviates-depressive-like-behavior-in-rats-submitted-to-repeated-lipopolysaccharide
#14
Ruili Dang, Xueyuan Zhou, Mimi Tang, Pengfei Xu, Xiaoxue Gong, Yuanyuan Liu, Hongxiao Jiao, Pei Jiang
PURPOSE: Depression is frequently associated with inflammation, whereas omega-3 polyunsaturated fatty acids (PUFAs) primarily found in fish oil possess anti-inflammatory properties. Although converging studies suggest an antidepressant effect of PUFAs, there is limited evidence directly linking the neuro-immune modulating features of PUFAs to the antidepressant actions. METHODS: Therefore, we assessed the effects of fish oil (FO) supplementation on behavioral changes, inflammatory cytokine expression and oxidative reactions in frontal cortex and hippocampus of rats following repeated peripheral immune challenge by lipopolysaccharide (LPS) for 2 weeks (500 μg/kg every other day)...
January 5, 2017: European Journal of Nutrition
https://www.readbyqxmd.com/read/28019679/inflammasome-activation-and-innate-immunity-in-alzheimer-s-disease
#15
Michael T Heneka
Activation of innate immunity and the assembly of microglial cells at sites of Alzheimer disease pathology has long been regarded as bystander phenomenon, which does not actively contribute to disease pathogenesis and progression. Recent data emerging from genetics, clinical imaging and animal experimentation point to an intimate and mutual interaction of innate immune mechanisms and neurodegenerative processes. NOD-like receptor (NLR) family, pyrin domain containing 3 and 1 inflammasomes, present in myeloid cells and neurons, respectively, represent key components of the innate immune reaction observed in Alzheimer patient brains...
March 2017: Brain Pathology
https://www.readbyqxmd.com/read/28009081/mini-symposium-role-of-the-inflammasome-in-brain-pathogenesis-a-potential-therapeutic-target-introduction
#16
Delphine Boche, David Brough
No abstract text is available yet for this article.
March 2017: Brain Pathology
https://www.readbyqxmd.com/read/28003153/inhibiting-the-nlrp3-inflammasome-with-mcc950-promotes-non-phlogistic-clearance-of-amyloid-%C3%AE-and-cognitive-function-in-app-ps1-mice
#17
C Dempsey, A Rubio Araiz, K J Bryson, O Finucane, C Larkin, E L Mills, A A B Robertson, M A Cooper, L A J O'Neill, M A Lynch
Activation of the inflammasome is implicated in the pathogenesis of an increasing number of inflammatory diseases, including Alzheimer's disease (AD). Research reporting inflammatory changes in post mortem brain tissue of individuals with AD and GWAS data have convincingly demonstrated that neuroinflammation is likely to be a key driver of the disease. This, together with the evidence that genetic variants in the NLRP3 gene impact on the risk of developing late-onset AD, indicates that targetting inflammation offers a therapeutic opportunity...
December 18, 2016: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/27997059/a-brain-in-flame-do-inflammasomes-and-pyroptosis-influence-stroke-pathology
#18
Jack Barrington, Eloise Lemarchand, Stuart M Allan
Stroke is one of the leading causes of death and disability worldwide. Inflammation plays a key role across the time course of stroke, from onset to the post-injury reparative phase days to months later. Several regulatory molecules are implicated in inflammation, but the most established inflammatory mediator of acute brain injury is the cytokine interleukin-1. Interleukin-1 is regulated by large, macromolecular complexes called inflammasomes, which play a central role in cytokine release and cell death. In this review we highlight recent advances in inflammasome research and propose key roles for inflammasome components in the progression of stroke damage...
March 2017: Brain Pathology
https://www.readbyqxmd.com/read/27997042/what-do-we-know-about-the-inflammasome-in-humans
#19
Jay Amin, Delphine Boche, Sonja Rakic
The inflammasome complex is part of the innate immune system, which serves to protect the host against harm from pathogens and damaged cells. It is a term first proposed by Tschopp's group in 2002, with numerous original research articles and reviews published on the topic since. There have been many types of inflammasome identified, but all result in the common pathway of activation of caspases and interleukin 1β along with possible cell death called pyroptosis. Despite a growing body of research investigating the structure and function of the inflammasome in animal models, there is still limited evidence identifying inflammasome components in human physiology and disease...
March 2017: Brain Pathology
https://www.readbyqxmd.com/read/27981190/stress-induced-neuroinflammatory-priming-a-liability-factor-in-the-etiology-of-psychiatric-disorders
#20
REVIEW
Matthew G Frank, Michael D Weber, Linda R Watkins, Steven F Maier
Stress and glucocorticoids (GCs) have universally been considered to be anti-inflammatory, however in recent years, stress and GCs have been found to exert permissive effects (immunological priming) on neuroinflammatory processes. This phenomenon of priming is characterized by prior stress or GC exposure potentiating the neuroinflammatory response to a subsequent immune challenge. A considerable body of evidence is discussed here that supports this permissive effect of stress and GCs. In light of this evidence, a mechanism of neuroinflammatory priming is proposed involving a signal cascade in the brain involving danger-associated molecular patterns (HMGB-1) and inflammasomes (NLRP3), which results in an exaggerated or amplified neuroinflammatory response and subsequently, the amplification of the physiological and behavioral sequelae of this response (i...
October 2016: Neurobiology of Stress
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