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Inflammasome microglia

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https://www.readbyqxmd.com/read/29670611/advances-in-biomarker-guided-therapy-for-pediatric-and-adult-onset-neuroinflammatory-disorders-targeting-chemokines-cytokines
#1
REVIEW
Michael R Pranzatelli
The concept and recognized components of "neuroinflammation" are expanding at the intersection of neurobiology and immunobiology. Chemokines (CKs), no longer merely necessary for immune cell trafficking and positioning, have multiple physiologic, developmental, and modulatory functionalities in the central nervous system (CNS) through neuron-glia interactions and other mechanisms affecting neurotransmission. They issue the "help me" cry of neurons and astrocytes in response to CNS injury, engaging invading lymphoid cells (T cells and B cells) and myeloid cells (dendritic cells, monocytes, and neutrophils) (adaptive immunity), as well as microglia and macrophages (innate immunity), in a cascade of events, some beneficial (reparative), others destructive (excitotoxic)...
2018: Frontiers in Immunology
https://www.readbyqxmd.com/read/29666475/lincrna-cox2-regulates-nlrp3-inflammasome-and-autophagy-mediated-neuroinflammation
#2
Zhenyi Xue, Zimu Zhang, Hongkun Liu, Wen Li, Xiangdong Guo, Zhihui Zhang, Ying Liu, Long Jia, Yan Li, Yinghui Ren, Hongwei Yang, Lijuan Zhang, Qi Zhang, Yurong Da, Junwei Hao, Zhi Yao, Rongxin Zhang
Inflammasome activation plays key roles in host defense, but also contributes to the pathogenesis of auto-inflammatory, and neurodegenerative diseases. As autophagy is connected with both the innate and adaptive immune systems, autophagic dysfunction is also closely related to inflammation, infection, and neurodegeneration. Here we identify that lincRNA-Cox2, previously known as a mediator of both the activation and repression of immune genes expression in innate immune cells, could bind NF-κB p65 and promote its nuclear translocation and transcription, modulating the expression of inflammasome sensor NLRP3 and adaptor ASC...
April 17, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29665074/parkin-deficiency-modulates-nlrp3-inflammasome-activation-by-attenuating-an-a20-dependent-negative-feedback-loop
#3
François Mouton-Liger, Thibault Rosazza, Julia Sepulveda-Diaz, Amélie Ieang, Sidi-Mohamed Hassoun, Emilie Claire, Graziella Mangone, Alexis Brice, Patrick P Michel, Jean-Christophe Corvol, Olga Corti
Neuroinflammation and mitochondrial dysfunction, key mechanisms in the pathogenesis of Parkinson's disease (PD), are usually explored independently. Loss-of-function mutations of PARK2 and PARK6, encoding the E3 ubiquitin protein ligase Parkin and the mitochondrial serine/threonine kinase PINK1, account for a large proportion of cases of autosomal recessive early-onset PD. PINK1 and Parkin regulate mitochondrial quality control and have been linked to the modulation of innate immunity pathways. We report here an exacerbation of NLRP3 inflammasome activation by specific inducers in microglia and bone marrow-derived macrophages from Park2-/- and Pink1-/- mice...
April 17, 2018: Glia
https://www.readbyqxmd.com/read/29618797/development-of-a-characterised-tool-kit-for-the-interrogation-of-nlrp3-inflammasome-dependent-responses
#4
Elena Redondo-Castro, Dorte Faust, Simon Fox, Alex G Baldwin, Simon Osborne, Michael J Haley, Eric Karran, Hugh Nuthall, Peter J Atkinson, Lee A Dawson, Carol Routledge, Stuart M Allan, Sally Freeman, Janet Brownlees, David Brough
Inflammation is an established contributor to disease and the NLRP3 inflammasome is emerging as a potential therapeutic target. A number of small molecule inhibitors of the NLRP3 pathway have been described. Here we analysed the most promising of these inhibitor classes side by side to assess relative potency and selectivity for their respective putative targets. Assessed using ASC inflammasome-speck formation, and release of IL-1β, in both human monocyte/macrophage THP1 cells and in primary mouse microglia, we compared the relative potency and selectivity of P2X7 inhibitors, inflammasome inhibitors (diarylsulfonylurea vs...
April 4, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29522854/chronic-amyloid-%C3%AE-oligomer-infusion-evokes-sustained-inflammation-and-microglial-changes-in-the-rat-hippocampus-via-nlrp3
#5
Csaba Fekete, Csaba Vastagh, Ádám Dénes, Erik Hrabovszky, Gábor Nyiri, Imre Kalló, Zsolt Liposits, Miklós Sárvári
Microglia are instrumental for recognition and elimination of amyloid β1-42 oligomers (AβO), but the long-term consequences of AβO-induced inflammatory changes in the brain are unclear. Here, we explored microglial responses and transciptome-level inflammatory signatures in the rat hippocampus after chronic AβO challenge. Middle-aged Long Evans rats received intracerebroventricular infusion of AβO or vehicle for 4 weeks, followed by treatment with artificial CSF or MCC950 for the subsequent 4 weeks. AβO infusion evoked a sustained inflammatory response including activation of NF-κB, triggered microglia activation and increased the expression of pattern recognition and phagocytic receptors...
March 6, 2018: Neuroscience
https://www.readbyqxmd.com/read/29492824/inflammasome-activation-by-methamphetamine-potentiates-lipopolysaccharide-stimulation-of-il-1%C3%AE-production-in-microglia
#6
Enquan Xu, Jianuo Liu, Han Liu, Xiaobei Wang, Huangui Xiong
Methamphetamine (Meth) is an addictive psychostimulant abused worldwide. Ample evidence indicate that chronic abuse of Meth induces neurotoxicity via microglia-associated neuroinflammation and the activated microglia present in both Meth-administered animals and human abusers. The development of anti-neuroinflammation as a therapeutic strategy against Meth dependence promotes research to identify inflammatory pathways that are specifically tied to Meth-induced neurotoxicity. Currently, the exact mechanisms for Meth-induced microglia activation are largely unknown...
February 28, 2018: Journal of Neuroimmune Pharmacology: the Official Journal of the Society on NeuroImmune Pharmacology
https://www.readbyqxmd.com/read/29439605/microglial-inflammasome-activation-in-penetrating-ballistic-like-brain-injury
#7
Stephanie W Lee, Shyam Gajavelli, Markus S Spurlock, Cody Andreoni, Juan Pablo de Rivero Vaccari, M Ross Bullock, Robert W Keane, W Dalton Dietrich
Penetrating traumatic brain injury (PTBI) is a significant cause of death and disability in the United States. Inflammasomes are one of the key regulators of the interleukin (IL)-1β mediated inflammatory responses after traumatic brain injury (TBI). However, the contribution of inflammasome signaling after PTBI has not been determined. In this study, adult male Sprague-Dawley rats were subjected to sham procedures or penetrating ballistic-like brain injury (PBBI) and sacrificed at various time points. Tissues were assessed by immunoblot analysis for expression of IL-1β, IL-18 and components of the inflammasome: apoptosis-associated speck-like protein containing a caspase-activation and recruitment domain (ASC), caspase-1, X-linked inhibitor of apoptosis protein (XIAP), NOD-like receptor protein 3 (NLRP3), and gasdermin-D (GSDMD)...
February 14, 2018: Journal of Neurotrauma
https://www.readbyqxmd.com/read/29434227/the-nlrp3-inflammasome-may-contribute-to-pathologic-neovascularization-in-the-advanced-stages-of-diabetic-retinopathy
#8
Shyam S Chaurasia, Rayne R Lim, Bhav H Parikh, Yeo Sia Wey, Bo Bo Tun, Tien Yin Wong, Chi D Luu, Rupesh Agrawal, Arkasubhra Ghosh, Alessandra Mortellaro, Elizabeth Rackoczy, Rajiv R Mohan, Veluchamy A Barathi
Diabetic retinopathy (DR) is a retinal microvascular disease characterized by inflammatory and angiogenic pathways. In this study, we evaluated NLRP3 inflammasome in a double transgenic mouse model, Akimba (Ins2 Akita xVEGF +/- ), which demonstrates hyperglycemia, vascular hyperpermeability and neovascularization seen in the proliferative DR. Retinal structural integrity, vascular leakage and function were examined by fundus photography, fluorescein angiography, optical coherence tomography, retinal flat mounts, laser speckle flowgraphy (LSFG), and electroretinography in Akimba and its parental strains, Akita (Ins2 Akita ) and Kimba (trVEGF029) mice...
February 12, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29396515/blockade-of-microglial-adenosine-a2a-receptor-impacts-inflammatory-mechanisms-reduces-arpe-19-cell-dysfunction-and-prevents-photoreceptor-loss-in-vitro
#9
M H Madeira, K Rashid, A F Ambrósio, A R Santiago, T Langmann
Age-related macular degeneration (AMD) is characterized by pathological changes in the retinal pigment epithelium (RPE) and loss of photoreceptors. Growing evidence has demonstrated that reactive microglial cells trigger RPE dysfunction and loss of photoreceptors, and inflammasome pathways and complement activation contribute to AMD pathogenesis. We and others have previously shown that adenosine A2A receptor (A2AR) blockade prevents microglia-mediated neuroinflammatory processes and mediates protection to the retina...
February 2, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29343269/microglial-activation-mediates-chronic-mild-stress-induced-depressive-and-anxiety-like-behavior-in-adult-rats
#10
Ya-Lin Wang, Qiu-Qin Han, Wen-Qing Gong, Dong-Hui Pan, Li-Zheng Wang, Wei Hu, Min Yang, Bing Li, Jin Yu, Qiong Liu
BACKGROUND: Depression is a heterogeneous disorder, with the exact neuronal mechanisms causing the disease yet to be discovered. Recent work suggests it is accompanied by neuro-inflammation, characterized, in particular, by microglial activation. However, microglial activation and its involvement in neuro-inflammation and stress-related depressive disorders are far from understood. METHODS: We utilized multiple detection methods to detect the neuro-inflammation in the hippocampus of rats after exposure to chronic mild stress (CMS)...
January 17, 2018: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/29318480/rosmarinic-acid-mitigates-lipopolysaccharide-induced-neuroinflammatory-responses-through-the-inhibition-of-tlr4-and-cd14-expression-and-nf-%C3%AE%C2%BAb-and-nlrp3-inflammasome-activation
#11
Yicong Wei, Jianxiong Chen, Yonghong Hu, Wei Lu, Xiaoqin Zhang, Ruiguo Wang, Kedan Chu
The excessive activation of microglia plays a key role in the pathogenesis of neurodegenerative diseases. The neuroprotective properties of rosmarinic acid have been reported in a variety of disease models both in vitro and in vivo; however, the mechanism underlying its anti-neuroinflammatory activity has not been clearly elucidated. In the present study, we evaluated the anti-inflammatory effects of rosmarinic acid in conditions of neuroinflammatory injury in vitro and in vivo. The results indicated that rosmarinic acid reduced the expression of CD11b, a marker of microglia and macrophages, in the brain and dramatically inhibited the levels of inflammatory cytokines and mediators, such as TNFα, IL-6, IL-1β, COX-2, and iNOS, in a dose-dependent manner both in vitro and in vivo...
March 2018: Inflammation
https://www.readbyqxmd.com/read/29306934/gliotransmitters-and-cytokines-in-the-control-of-blood-brain-barrier-permeability
#12
REVIEW
Elena D Osipova, Oxana V Semyachkina-Glushkovskaya, Andrey V Morgun, Natalia V Pisareva, Natalia A Malinovskaya, Elizaveta B Boitsova, Elena A Pozhilenkova, Olga A Belova, Vladimir V Salmin, Tatiana E Taranushenko, Mami Noda, Alla B Salmina
The contribution of astrocytes and microglia to the regulation of neuroplasticity or neurovascular unit (NVU) is based on the coordinated secretion of gliotransmitters and cytokines and the release and uptake of metabolites. Blood-brain barrier (BBB) integrity and angiogenesis are influenced by perivascular cells contacting with the abluminal side of brain microvessel endothelial cells (pericytes, astrocytes) or by immune cells existing (microglia) or invading the NVU (macrophages) under pathologic conditions...
January 8, 2018: Reviews in the Neurosciences
https://www.readbyqxmd.com/read/29304864/hypercapnia-induces-il-1%C3%AE-overproduction-via-activation-of-nlrp3-inflammasome-implication-in-cognitive-impairment-in-hypoxemic-adult-rats
#13
Hong-Guang Ding, Yi-Yu Deng, Ren-Qiang Yang, Qiao-Sheng Wang, Wen-Qiang Jiang, Yong-Li Han, Lin-Qiang Huang, Miao-Yun Wen, Wen-Hong Zhong, Xu-Sheng Li, Fan Yang, Hong-Ke Zeng
BACKGROUND: Cognitive impairment is one of common complications of acute respiratory distress syndrome (ARDS). Increasing evidence suggests that interleukin-1 beta (IL-1β) plays a role in inducing neuronal apoptosis in cognitive dysfunction. The lung protective ventilatory strategies, which serve to reduce pulmonary morbidity for ARDS patients, almost always lead to hypercapnia. Some studies have reported that hypercapnia contributes to the risk of cognitive impairment and IL-1β secretion outside the central nervous system (CNS)...
January 5, 2018: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/29301581/activation-of-dopamine-d1-receptor-decreased-nlrp3-mediated-inflammation-in-intracerebral-hemorrhage-mice
#14
Tian Wang, Derek Nowrangi, Lingyan Yu, Tai Lu, Jiping Tang, Bing Han, Yuxin Ding, Fenghua Fu, John H Zhang
BACKGROUND: Inflammasomes are involved in diverse inflammatory diseases. Previous study reported that the neurotransmitter dopamine inhibited NLRP3 inflammasome activation via dopamine D1 receptor (DRD1). The present study aims to investigate the role of DRD1 on neuroinflammation in intracerebral hemorrhage (ICH) mice and the potential mechanism mediated by NLRP3 inhibition. METHODS: One hundred and six male CD-1 mice were subjected to intrastriatal injection of bacterial collagenase or PBS...
January 4, 2018: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/29290552/microglial-ramification-surveillance-and-interleukin-1%C3%AE-release-are-regulated-by-the-two-pore-domain-k-channel-thik-1
#15
Christian Madry, Vasiliki Kyrargyri, I Lorena Arancibia-Cárcamo, Renaud Jolivet, Shinichi Kohsaka, Robert M Bryan, David Attwell
Microglia exhibit two modes of motility: they constantly extend and retract their processes to survey the brain, but they also send out targeted processes to envelop sites of tissue damage. We now show that these motility modes differ mechanistically. We identify the two-pore domain channel THIK-1 as the main K+ channel expressed in microglia in situ. THIK-1 is tonically active, and its activity is potentiated by P2Y12 receptors. Inhibiting THIK-1 function pharmacologically or by gene knockout depolarizes microglia, which decreases microglial ramification and thus reduces surveillance, whereas blocking P2Y12 receptors does not affect membrane potential, ramification, or surveillance...
January 17, 2018: Neuron
https://www.readbyqxmd.com/read/29273951/neuroinflammatory-responses-in-alzheimer-s-disease
#16
REVIEW
Cira Dansokho, Michael Thomas Heneka
Neuroinflammatory responses in Alzheimer's disease (AD) are complex and not fully understood. They involve various cellular and molecular players and associate interaction between the central nervous system (CNS) and the periphery. Amyloid peptides within the senile plaques and abnormally phosphorylated tau in neurofibrillary tangles are able to initiate inflammatory responses, in brain of AD patients and in mouse models of this disease. The outcome of these responses on the pathophysiology of AD depends on several factors and can be either beneficial or detrimental...
December 22, 2017: Journal of Neural Transmission
https://www.readbyqxmd.com/read/29219210/bioenergetic-regulation-of-microglia
#17
REVIEW
Soumitra Ghosh, Erika Castillo, Elma S Frias, Raymond A Swanson
Microglia have diverse actions, ranging from synapse pruning in development to cytotoxic effects in disease. Brain energy metabolism and substrate availability vary under normal and disease states, but how these variations influence microglial function is relatively unknown. Microglia, like most other cell types, express the full complement of gene products required for both glycolytic and oxidative metabolism. Evidence suggests that microglia increase aerobic glycolysis and decrease respiration when activated by various stimuli...
December 8, 2017: Glia
https://www.readbyqxmd.com/read/29212744/selective-nlrp3-pyrin-domain-containing-protein-3-inflammasome-inhibitor-reduces-brain-injury-after-intracerebral-hemorrhage
#18
Honglei Ren, Ying Kong, Zhijia Liu, Dongyun Zang, Xiaoxia Yang, Kristofer Wood, Minshu Li, Qiang Liu
BACKGROUND AND PURPOSE: Intracerebral hemorrhage (ICH) is a devastating disease without effective treatment. As a key component of the innate immune system, the NOD-like receptor (NLR) family, NLRP3 (pyrin domain-containing protein 3) inflammasome, when activated after ICH, promotes neuroinflammation and brain edema. MCC950 is a potent, selective, small-molecule NLRP3 inhibitor that blocks NLRP3 activation at nanomolar concentrations. Here, we examined the effect of MCC950 on brain injury and inflammation in 2 models of ICH in mice...
January 2018: Stroke; a Journal of Cerebral Circulation
https://www.readbyqxmd.com/read/29196167/cathepsin-b-links-oxidative-stress-to-the-activation-of-nlrp3-inflammasome
#19
Hua Bai, Bo Yang, Wenfeng Yu, Yan Xiao, Dejun Yu, Qifang Zhang
Oxidative stress-mediated activation of NLRP3 inflammasome in microglia is critical in the development of neurodegerative diseases such as Alzheimer's disease (AD), Parkinson disease (PD). However, the mechanism underlying oxidative stress activates NLRP3 inflammasome remains exclusive. Here we demonstrated cathepsin B (CTSB) as a regulator of the activation of NLRP3 inflammasome by H2 O2 ·H2 O2 induced IL-1β secretion in NLRP3 inflammasome-dependent manner·H2 O2 treatment increased CTSB activity, which in turn activated NLRP3 inflammasome, and subsequently processed pro-caspase-1 cleavage into caspase-1, resulting in IL-1 β secretion...
January 1, 2018: Experimental Cell Research
https://www.readbyqxmd.com/read/29191728/the-sp-2-iminosugar-glycolipid-1-dodecylsulfonyl-5n-6o-oxomethylidenenojirimycin-dso-2-onj-as-selective-anti-inflammatory-agent-by-modulation-of-hemeoxygenase-1-in-bv-2-microglial-cells-and-retinal-explants
#20
Elena Alcalde-Estévez, Ana I Arroba, Elena M Sánchez-Fernández, Carmen Ortiz Mellet, Jose M García Fernández, Laura Masgrau, Ángela M Valverde
Neuroinflammation is an early event during diabetic retinopathy (DR) that impacts the dynamics of microglia polarization. Gliosis is a hallmark of DR and we have reported the beneficial effects of 1R-DSO-ONJ, a member of the sp2 -iminosugar glycolipid (sp2 -IGL) family, in targeting microglia and reducing gliosis in diabetic db/db mice. Herein, we analyzed the effect of DSO2 -ONJ, another family compound incorporating a sulfone group that better mimics the phosphate group of phosphatidylinositol ether lipid analogues (PIAs), in Bv...
January 2018: Food and Chemical Toxicology
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