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Inflammasome brain

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https://www.readbyqxmd.com/read/28077335/omega-3-fatty-acids-regulate-nlrp3-inflammasome-activation-and-prevent-behavior-deficits-after-traumatic-brain-injury
#1
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
#2
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
#3
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...
December 26, 2016: Brain Pathology
https://www.readbyqxmd.com/read/28009081/role-of-the-inflammasome-in-brain-pathogenesis-a-potential-therapeutic-target
#4
Delphine Boche, David Brough
No abstract text is available yet for this article.
December 23, 2016: 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
#5
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
#6
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...
December 20, 2016: Brain Pathology
https://www.readbyqxmd.com/read/27997042/what-do-we-know-about-the-inflammasome-in-humans
#7
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 due to 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...
December 20, 2016: Brain Pathology
https://www.readbyqxmd.com/read/27981190/stress-induced-neuroinflammatory-priming-a-liability-factor-in-the-etiology-of-psychiatric-disorders
#8
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
https://www.readbyqxmd.com/read/27933491/nlrp3-is-required-for-complement-mediated-caspase-1-and-il-1beta-activation-in-ich-short-title-for-running-head-nlrp3-is-required-for-ich
#9
Sheng-Tao Yao, Fang Cao, Jia-Lin Chen, Wei Chen, Rui-Ming Fan, Gang Li, You-Chao Zeng, Song Jiao, Xiang-Ping Xia, Chong Han, Qi-Shan Ran
Complement-mediated inflammation plays a vital role in intracerebral hemorrhage (ICH), implicating pro-inflammatory factor interleukin-1beta (IL-1β) secretion. Brain samples and contralateral hemiencephalon were all collected and detected by Western blot. NLRP3 expression was located by dual immunofluorescence staining at 1, 3, and 5 days post-ICH. Brain water content was examined post-ICH. The neural deficit scores were evaluated by observers blindly. ILs were detected by ELISA. SiRNAs targeting NLRP3 (siNLRP3), siASC, and siControl were injected to inhibit NLRP3 function...
December 8, 2016: Journal of Molecular Neuroscience: MN
https://www.readbyqxmd.com/read/27924425/inhibition-of-nlrp3-inflammasome-prevents-lps-induced-inflammatory-hyperalgesia-in-mice-contribution-of-nf-%C3%AE%C2%BAb-caspase-1-11-asc-nox-and-nos-isoforms
#10
Abdurrahman Dolunay, Sefika Pinar Senol, Meryem Temiz-Resitoglu, Demet Sinem Guden, Ayse Nihal Sari, Seyhan Sahan-Firat, Bahar Tunctan
The nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3), an intracellular signaling molecule that senses many environmental- and pathogen/host-derived factors, has been implicated in the pathogenesis of several diseases associated with inflammation. It has been suggested that NLRP3 inflammasome inhibitors may have a therapeutic potential in the treatment of NLRP3-related inflammatory diseases. The aim of this study was to determine whether inhibition of NLRP3 inflammasome prevents inflammatory hyperalgesia induced by lipopolysaccharide (LPS) in mice as well as changes in expression/activity of nuclear factor κB (NF-κB), caspase-1/11, nicotinamide adenine dinucleotide phosphate oxidase (NOX), and endothelial/neuronal/inducible nitric oxide synthase (eNOS/nNOS/iNOS) that may regulate NLRP3/apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC)/pro-caspase-1 inflammasome formation and activity by using a selective NLRP3 inflammasome inhibitor, MCC950...
December 6, 2016: Inflammation
https://www.readbyqxmd.com/read/27923741/nlrp3-inflammasome-activation-contributes-to-long-term-behavioral-alterations-in-mice-injected-with-lipopolysaccharide
#11
Wei Zhu, Feng-Sheng Cao, Jun Feng, Hua-Weng Chen, Jie-Ru Wan, Qing Lu, Jian Wang
Lipopolysaccharide (LPS) might affect the central nervous system by causing neuroinflammation, which subsequently leads to brain damage and dysfunction. In this study, we evaluated the role of nod-like receptor pyrin domain-containing protein 3 (NLRP3) inflammasome activation in long-term behavioral alterations of 8-week-old male C57BL/6 mice injected intraperitoneally with LPS (5mg/kg). At different time points after injection, we assessed locomotor function with a 24-point neurologic deficit scoring system and the rotarod test; assessed recognition memory with the novel object recognition test; and assessed emotional abnormality (anhedonia and behavioral despair) with the tail suspension test, forced swim test, and sucrose preference test...
December 5, 2016: Neuroscience
https://www.readbyqxmd.com/read/27884375/the-inflammasome-friend-or-foe-in-chlamydia-infection
#12
EDITORIAL
Emma Louise Walton
In this issue of the Biomedical Journal, we take a look at the still somewhat perplexing role of the inflammasome in Chlamydia infection. We also highlight findings suggesting a link between structural changes to arteries in the brain and the onset of depression. Finally, we learn about some of the implications of co-morbidity between diabetes and infectious diseases.
October 2016: Biomedical Journal
https://www.readbyqxmd.com/read/27862491/alarmins-and-central-nervous-system-inflammation-in-hiv-associated-neurological-disorders
#13
M-L Gougeon
In the era of highly active antiretroviral therapy (HAART), HIV-1-associated neurocognitive disorders (HAND) persist in infected individuals with adequate immunological and virological status. Risk factors for cognitive impairment include hepatitis C virus co-infection, host genetic factors predisposing to HAND, the early establishment of the virus in the CNS and its persistence under HAART; thus, the CNS is an important reservoir for HIV. Microglial cells are permissive to HIV-1, and NLRP3 inflammasome-associated genes were found expressed in brains of HIV-1-infected persons, contributing to brain disease...
November 16, 2016: Journal of Internal Medicine
https://www.readbyqxmd.com/read/27862176/inflammasomes-hormesis-and-antioxidants-in-neuroinflammation-role-of-nrlp3-in-alzheimer-disease
#14
REVIEW
Manuela Pennisi, Rosalia Crupi, Rosanna Di Paola, Maria Laura Ontario, Rita Bella, Edward J Calabrese, Roberto Crea, Salvatore Cuzzocrea, Vittorio Calabrese
Alzheimer disease (AD) is a progressive neurodegenerative disorder leading to cognitive decline, neuropsychiatric symptoms, disability, caregiver burden, and premature death. It represents the most prevalent cause of dementia, and its incidence rates exponentially increase with increasing age. The number of Americans living with AD is rapidly increasing. An estimated 5.4 million Americans of all ages have AD in 2016. One in nine people aged 65 and older has AD, and by midcentury, someone in the United States will develop the disease every 33 sec...
November 8, 2016: Journal of Neuroscience Research
https://www.readbyqxmd.com/read/27846628/minocycline-suppresses-nlrp3-inflammasome-activation-in-experimental-ischemic-stroke
#15
Yunnan Lu, Guodong Xiao, Weifeng Luo
OBJECTIVE: Minocycline, a tetracycline antibiotic, has shown anti-inflammatory effects in cerebral ischemia and neurodegenerative disease; however, the molecular mechanisms underlying this effect have not been clearly identified. Since NLRP3 inflammasome activation controls the maturation and release of proinflammatory cytokines, especially interleukin-1β (IL-1β) and IL-18 in ischemia stroke, we suppose that minocycline may be involved in the regulation of NLRP3 inflammasome activation...
November 16, 2016: Neuroimmunomodulation
https://www.readbyqxmd.com/read/27843532/nlrp3-inflammasome-activation-in-the-brain-after-global-cerebral-ischemia-and-regulation-by-17%C3%AE-estradiol
#16
Roshni Thakkar, Ruimin Wang, Gangadhara Sareddy, Jing Wang, Dharma Thiruvaiyaru, Ratna Vadlamudi, Quanguang Zhang, Darrell Brann
17β-Estradiol (E2) is a well-known neuroprotective factor in the brain. Recently, our lab demonstrated that the neuroprotective and cognitive effects of E2 require mediation by the estrogen receptor (ER) coregulator protein and proline-, glutamic acid-, and leucine-rich protein 1 (PELP1). In the current study, we examined whether E2, acting via PELP1, can exert anti-inflammatory effects in the ovariectomized rat and mouse hippocampus to regulate NLRP3 inflammasome activation after global cerebral ischemia (GCI)...
2016: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/27832633/increased-cerebral-tff1-expression-in-two-murine-models-of-neuroinflammation
#17
Eva B Znalesniak, Ting Fu, Karina Guttek, Ulrike Händel, Dirk Reinhold, Werner Hoffmann
BACKGROUND/AIMS: The trefoil factor family (TFF) peptide TFF1 is a typical secretory product of the gastric mucosa and a very low level of expression occurs in nearly all regions of the murine brain. TFF1 possesses a lectin activity and binding to a plethora of transmembrane glycoproteins could explain the diverse biological effects of TFF1 (e.g., anti-apoptotic effect). It was the aim to test whether TFF expression is changed during neuroinflammation. METHODS: Expression profiling was performed using semi-quantitative RT-PCR analyses in two murine models of neuroinflammation, i...
2016: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/27826689/%C3%AE-hydroxybutyrate-in-the-brain-one-molecule-multiple-mechanisms
#18
Lavanya B Achanta, Caroline D Rae
β-Hydroxybutyrate (βOHB), a ketone body, is oxidised as a brain fuel. Although its contribution to energy metabolism in the healthy brain is minimal, it is an interesting metabolite which is not only oxidised but also has other direct and collateral effects which make it a molecule of interest for therapeutic purposes. In brain βOHB can be produced in astrocytes from oxidation of fatty acids or catabolism of amino acids and is metabolised in the mitochondria of all brain cell types although uptake across the blood brain barrier is a metabolic control point...
November 8, 2016: Neurochemical Research
https://www.readbyqxmd.com/read/27779191/25-hydroxycholesterol-contributes-to-cerebral-inflammation-of-x-linked-adrenoleukodystrophy-through-activation-of-the-nlrp3-inflammasome
#19
Jiho Jang, Sangjun Park, Hye Jin Hur, Hyun-Ju Cho, Inhwa Hwang, Yun Pyo Kang, Isak Im, Hyunji Lee, Eunju Lee, Wonsuk Yang, Hoon-Chul Kang, Sung Won Kwon, Je-Wook Yu, Dong-Wook Kim
X-linked adrenoleukodystrophy (X-ALD), caused by an ABCD1 mutation, is a progressive neurodegenerative disorder associated with the accumulation of very long-chain fatty acids (VLCFA). Cerebral inflammatory demyelination is the major feature of childhood cerebral ALD (CCALD), the most severe form of ALD, but its underlying mechanism remains poorly understood. Here, we identify the aberrant production of cholesterol 25-hydroxylase (CH25H) and 25-hydroxycholesterol (25-HC) in the cellular context of CCALD based on the analysis of ALD patient-derived induced pluripotent stem cells and ex vivo fibroblasts...
October 25, 2016: Nature Communications
https://www.readbyqxmd.com/read/27776263/association-of-brain-amyloidosis-with-pro-inflammatory-gut-bacterial-taxa-and-peripheral-inflammation-markers-in-cognitively-impaired-elderly
#20
Annamaria Cattaneo, Nadia Cattane, Samantha Galluzzi, Stefania Provasi, Nicola Lopizzo, Cristina Festari, Clarissa Ferrari, Ugo Paolo Guerra, Barbara Paghera, Cristina Muscio, Angelo Bianchetti, Giorgio Dalla Volta, Marinella Turla, Maria Sofia Cotelli, Michele Gennuso, Alessandro Prelle, Orazio Zanetti, Giulia Lussignoli, Dario Mirabile, Daniele Bellandi, Simona Gentile, Gloria Belotti, Daniele Villani, Taoufiq Harach, Tristan Bolmont, Alessandro Padovani, Marina Boccardi, Giovanni B Frisoni
The pathway leading from amyloid-β deposition to cognitive impairment is believed to be a cornerstone of the pathogenesis of Alzheimer's disease (AD). However, what drives amyloid buildup in sporadic nongenetic cases of AD is still unknown. AD brains feature an inflammatory reaction around amyloid plaques, and a specific subset of the gut microbiota (GMB) may promote brain inflammation. We investigated the possible role of the GMB in AD pathogenesis by studying the association of brain amyloidosis with (1) GMB taxa with pro- and anti-inflammatory activity; and (2) peripheral inflammation in cognitively impaired patients...
January 2017: Neurobiology of Aging
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