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Inflammasome brain

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https://www.readbyqxmd.com/read/28302008/mitochondria-targeted-antioxidants-as-a-prospective-therapeutic-strategy-for-multiple-sclerosis
#1
Elena K Fetisova, Boris V Chernyak, Galina A Korshunova, Maria S Muntyan, Vladimir P Skulachev
BACKGROUND: Multiple sclerosis (MS) is one of the most widespread chronic neurological diseases that manifests itself by progressive demyelination in the central nervous system. The study of MS pathogenesis begins with the onset of the relapsing-remitting phase of the disease, which becomes apparent due to microglia activation, neuroinflammation and demyelination/remyelination in the white matter. The following progressive phase is accompanied by severe neurological symptoms when demyelination and neurodegeneration are spread to both gray and white matter...
March 16, 2017: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/28300164/role-of-purinergic-signaling-in-experimental-pneumococcal-meningitis
#2
Marco Zierhut, Susanne Dyckhoff, Ilias Masouris, Matthias Klein, Sven Hammerschmidt, Hans-Walter Pfister, Korcan Ayata, Marco Idzko, Uwe Koedel
Excessive neutrophilic inflammation contributes to brain pathology and adverse outcome in pneumococcal meningitis (PM). Recently, we identified the NLRP3 inflammasome/interleukin (IL)-1β pathway as a key driver of inflammation in PM. A critical membrane receptor for NLRP3 inflammasome activation is the ATP-activated P2 purinoceptor (P2R) P2X7. Thus, we hypothesized involvement of ATP and P2Rs in PM. The functional role of ATP was investigated in a mouse meningitis model using P2R antagonists. Brain expression of P2Rs was assessed by RT-PCR...
March 16, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28274860/purinergic-2x7-receptor-nlrp3-pathway-triggers-neuronal-apoptosis-after-ischemic-stroke-in-the-mouse
#3
Xinchun Ye, Tong Shen, Jinxia Hu, Liang Zhang, Yunshan Zhang, Lei Bao, Chengcheng Cui, Guoliang Jin, Kun Zan, Zuohui Zhang, Xinxin Yang, Hongjuan Shi, Jie Zu, Ming Yu, Chengjie Song, Yulan Wang, Suhua Qi, Guiyun Cui
Previous research has shown that Purinergic 2X7 receptor (P2X7R) and NLRP3 inflammasome contribute to the inflammatory activation. In this study, we investigated whether P2X7R/NLRP3 pathway is involved in the caspase-3 dependent neuronal apoptosis after ischemic stroke by using a focal cortex ischemic stroke model. The expressions of P2X7R, NLRP3 inflammsome components, and cleaved caspase-3 were significantly enhanced in the ischemic brain tissue after stroke. However, the expression of cleaved caspase-3 was significantly attenuated after treatment of stroke with P2X7R antagonist (BBG) or NLRP3 inhibitor (MCC950)...
March 6, 2017: Experimental Neurology
https://www.readbyqxmd.com/read/28270571/hiv-1-tat-primes-and-activates-microglial-nlrp3-inflammasome-mediated-neuroinflammation
#4
Ernest T Chivero, Ming-Lei Guo, Palsamy Periyasamy, Ke Liao, Shannon E Callen, Shilpa Buch
Neuroinflammation associated with HIV-1 infection is a problem affecting ∼50% of HIV-infected individuals. NLRP3 inflammasome has been implicated in HIV-induced microglial activation, but the mechanism(s) remain unclear. Since HIV-Tat continues to be present despite antiretroviral therapy and activates NF-kB, we hypothesized that Tat could prime the NLRP3 inflammasome. We found a dose- and time-dependent induction of NLRP3 expression in microglia exposed to Tat compared with control. Tat exposure also time-dependently increased the mature caspase-1 and IL-1β levels and enhanced the IL-1β secretion...
March 7, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28263786/nlrp3-inflammasome-driven-pathways-in-depression-clinical-and-preclinical-findings
#5
REVIEW
Fernanda N Kaufmann, Ana Paula Costa, Gabriele Ghisleni, Alexandre P Diaz, Ana Lúcia S Rodrigues, Hugo Peluffo, Manuella P Kaster
Over the past three decades, an intricate interaction between immune activation, release of pro-inflammatory cytokines and changes in brain circuits related to mood and behavior has been described. Despite extensive efforts, questions regarding when inflammation becomes detrimental or how we can target the immune system to develop new therapeutic strategies for the treatment of psychiatric disorders remain unresolved. In this context, novel aspects of the neuroinflammatory process activated in response to stressful challenges have recently been documented in major depressive disorder (MDD)...
March 2, 2017: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/28255908/nlrp3-inflammasome-inhibitor-ameliorates-amyloid-pathology-in-a-mouse-model-of-alzheimer-s-disease
#6
Jun Yin, Fanpeng Zhao, Jeremy E Chojnacki, Jacob Fulp, William L Klein, Shijun Zhang, Xiongwei Zhu
The activation of the NLRP3 inflammasome signaling pathway plays an important role in the neuroinflammation in Alzheimer's disease (AD). In this study, we investigated the effects of JC-124, a rationally designed NLRP3 inflammasome inhibitor, on AD-related deficits in CRND8 APP transgenic mice (TgCRND8). We first demonstrated increased formation and activation of NLRP3 inflammasome in TgCRND8 mice compared to non-transgenic littermate controls, which was inhibited by the treatment with JC-124. Importantly, JC-124 treatment led to decreased levels of Aβ deposition and decreased levels of soluble and insoluble Aβ1-42 in the brain of CRND8 mice which was accompanied by reduced β-cleavage of APP, reduced activation of microglia but enhanced astrocytosis...
March 2, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28238167/effects-of-cox1-2-5-lox-blockade-in-alzheimer-transgenic-3xtg-ad-mice
#7
Alessandra Bitto, Daniela Giuliani, Giovanni Pallio, Natasha Irrera, Eleonora Vandini, Fabrizio Canalini, Davide Zaffe, Alessandra Ottani, Letteria Minutoli, Mariagrazia Rinaldi, Salvatore Guarini, Francesco Squadrito, Domenica Altavilla
OBJECTIVE AND DESIGN: Alzheimer's disease (AD) is associated with amyloid plaques (Aβ) and hyperphosphorylated tau protein tangles in the brain. We investigated the possible neuroprotective role of flavocoxid, a dual inhibitor of cyclooxygenases-1/2 (COX-1/2) and 5-Lipoxygenase (5-LOX), in triple-transgenic (3xTg-AD) mice. SUBJECTS: Mice were 3 months at the beginning of the study. TREATMENT: Animals received once daily for 3-month saline solution or flavocoxid (20 mg/kg/ip)...
February 25, 2017: Inflammation Research: Official Journal of the European Histamine Research Society ... [et Al.]
https://www.readbyqxmd.com/read/28202418/ros-txnip-pathway-contributes-to-thrombin-induced-nlrp3-inflammasome-activation-and-cell-apoptosis-in-microglia
#8
Xinchun Ye, Dandan Zuo, 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...
April 1, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28186177/the-far-reaching-scope-of-neuroinflammation-after-traumatic-brain-injury
#9
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
#10
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
#11
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
#12
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
#13
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
#14
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...
March 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28129888/alzheimer-s-disease-innate-immunity-gone-awry
#15
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...
April 2017: Metabolism: Clinical and Experimental
https://www.readbyqxmd.com/read/28129542/pathogen-mediated-inhibition-of-anorexia-promotes-host-survival-and-transmission
#16
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
#17
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
#18
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
#19
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
#20
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...
April 2017: Experimental Neurology
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