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Inflammasome microglia

Masaaki Iwata, Hisahito Ishida, Koichi Kaneko, Yukihiko Shirayama
An accumulating body of evidence has demonstrated that inflammation is associated with the pathology of depression. We recently found that psychological stress induces inflammation in the hippocampus of the rat brain through the inflammasome, a component of the innate immune system. Microglia, the resident macrophages in the brain, play a central role in the innate immune system and express inflammasomes; thus, we hypothesized that hippocampal microglia would be key mediators in the development of depression via stress-induced inflammation...
October 18, 2016: Pharmacology, Biochemistry, and Behavior
Jing Qiu, Min Wang, Jun Zhang, Qing Cai, Dan Lu, Yansong Li, Yushu Dong, Tianzhi Zhao, Huisheng Chen
Neuroinflammation remains the primary cause of morbidity and mortality in stroke-induced secondary brain injury. The NOD-like receptor pyrin 3 (NLRP3) inflammasome is involved in diverse inflammatory diseases, including cerebral ischemia, and is thus considered an effective therapeutic target. In the present study, we investigated the neuroprotection of Sinomenine (SINO), a potent natural anti-apoptotic and anti-inflammatory molecule, against cerebral ischemia in a mouse model of middle cerebral artery occlusion (MCAO) in vivo and in an oxygen glucose deprivation (OGD)-treated astrocytes/microglia model in vitro...
October 18, 2016: International Immunopharmacology
Kai-Chih Hung, Hui-Ju Huang, Yi-Ting Wang, Anya Maan-Yuh Lin
ETHNOPHARMACOLOGICAL RELEVANCE: Neuroinflammation, oxidative stress, and protein aggregation form a vicious cycle in the pathophysiology of Parkinson's disease (PD); activated microglia is the main location of neuroinflammation. A Chinese medicine book, "Shanghan Lun", known as the "Treatises on Cold damage Diseases" has suggested that Scutellaria baicalensis Georgi is effective in treating CNS diseases. The anti-inflammatory mechanisms of baicalein, a phenolic flavonoid in the dried root of Scutellaria baicalensis Georgi, remain to be explored...
October 11, 2016: Journal of Ethnopharmacology
Manmeet K Mamik, Elizabeth Hui, William G Branton, Brienne A McKenzie, Jesse Chisholm, Eric A Cohen, Christopher Power
Human Immunodeficiency virus (HIV) enters the brain soon after seroconversion and induces chronic neuroinflammation by infecting and activating brain macrophages. Inflammasomes are cytosolic protein complexes that mediate caspase-1 activation and ensuing cleavage and release of IL-1β and -18 by macrophages. Our group recently showed that HIV-1 infection of human microglia induced inflammasome activation in NLRP3-dependent manner. The HIV-1 viral protein R (Vpr) is an accessory protein that is released from HIV-infected cells, although its effects on neuroinflammation are undefined...
October 10, 2016: Journal of Neuroimmune Pharmacology: the Official Journal of the Society on NeuroImmune Pharmacology
F Guerriero, C Sgarlata, M Francis, N Maurizi, A Faragli, S Perna, M Rondanelli, M Rollone, G Ricevuti
Due to an increasingly aging population, Alzheimer disease (AD) represents a crucial issue for the healthcare system because of its widespread prevalence and the burden of its care needs. Several hypotheses on AD pathogenesis have been proposed and current therapeutical strategies have shown limited effectiveness. In the last decade, more evidence has supported a role for neuroinflammation and immune system dysregulation in AD. It remains unclear whether astrocytes, microglia and immune cells influence disease onset, progression or both...
October 7, 2016: Aging Clinical and Experimental Research
Jorge Montesinos, Silvia Alfonso-Loeches, Consuelo Guerri
The innate immune response in the central nervous system (CNS) participates in both synaptic plasticity and neural damage. Emerging evidence from human and animal studies supports the role of the neuroimmune system response in many actions of ethanol (EtOH) on the CNS. Research studies have shown that alcohol stimulates brain immune cells, microglia, and astrocytes, by activating innate immune receptors Toll-like receptors (TLRs) and NOD-like receptors (inflammasome NLRs) triggering signaling pathways, which culminate in the production of pro-inflammatory cytokines and chemokines that lead to neuroinflammation...
September 21, 2016: Alcoholism, Clinical and Experimental Research
Saskia Maria Burm, Ella Alwine Zuiderwijk-Sick, Paola Massiel Weert, Jeffrey John Bajramovic
Under stressful conditions nucleotides are released from dying cells into the extracellular space, where they can bind to purinergic P2X and P2Y receptors. High concentrations of extracellular ATP in particular induce P2X7-mediated signaling, which leads to inflammasome activation. This in turn leads to the processing and secretion of pro-inflammatory cytokines, like interleukin (IL)-1β. During neurodegenerative diseases, innate immune responses are shaped by microglia and we have previously identified microglia-specific features of inflammasome-mediated responses...
September 19, 2016: Glia
A D Dick
Dogma for reasons of immune privilege including sequestration (sic) of ocular antigen, lack of lymphatic and immune competent cells in the vital tissues of the eye has long evaporated. Maintaining tissue and cellular health to preserve vision requires active immune responses to prevent damage and respond to danger. A priori the eye must contain immune competent cells, undergo immune surveillance to ensure homoeostasis as well as an ability to promote inflammation. By interrogating immune responses in non-infectious uveitis and compare with age-related macular degeneration (AMD), new concepts of intraocular immune health emerge...
September 16, 2016: Eye
Yang Pan, Bo Shen, Qin Gao, Jun Zhu, Jingde Dong, Li Zhang, Yingdong Zhang
Neuroinflammation has been recognized as a factor in the pathogenesis of neurodegenerative diseases. Emerging evidence suggests that peripheral inflammation, besides neuroinflammation, functions as a modulator of disease progression and neuropathology in several neurodegenerative diseases. However, detailed correlations among peripheral inflammation, neuroinflammation and neurodegeneration remain unknown. In the present study, we prepared a peripheral inflammation model with lipopolysaccharides (LPS)-stimulated RAW264...
May 2016: Journal of Biomedical Research
Ana I Arroba, Lourdes Rodríguez-de la Rosa, Silvia Murillo-Cuesta, Laura Vaquero-Villanueva, Juan M Hurlé, Isabel Varela-Nieto, Ángela M Valverde
Insulin-like growth factor-1 (IGF-1) is a growth factor with differentiating, anti-apoptotic and metabolic functions in the periphery, and anti-inflammatory properties in the nervous system. Mice that have mutations in the Igf1 gene, rendering the gene product inactive (Igf1(-/-)), present with age-related visual loss accompanied by structural alterations in the first synapses of the retinal pathway. Recent advances have revealed a crucial role of autophagy in immunity and inflammation. Keeping in mind this close relationship, we aimed to decipher these processes in the context of the defects that occur during ageing in the retina of Igf1(-/-) mice...
September 1, 2016: Disease Models & Mechanisms
Philippe Leff-Gelman, Ismael Mancilla-Herrera, Mónica Flores-Ramos, Carlos Cruz-Fuentes, Juan Pablo Reyes-Grajeda, María Del Pilar García-Cuétara, Marielle Danitza Bugnot-Pérez, David Ellioth Pulido-Ascencio
Major depression during pregnancy is a common psychiatric disorder that arises from a complex and multifactorial etiology. Psychosocial stress, sex, hormones, and genetic vulnerability increase the risk for triggering mood disorders. Microglia and toll-like receptor 4 play a crucial role in triggering wide and varied stress-induced responses mediated through activation of the inflammasome; this leads to the secretion of inflammatory cytokines, increased serotonin metabolism, and reduction of neurotransmitter availability along with hypothalamic-pituitary-adrenal axis hyperactivity...
August 2016: Neuroscience Bulletin
Fernanda M Marim, Miriam M Costa Franco, Marco Tulio R Gomes, Maria Cruz Miraglia, Guillermo H Giambartolomei, Sergio Costa Oliveira
The innate immune system is essential for the detection and elimination of bacterial pathogens. Upon inflammasome activation, caspase-1 cleaves pro-IL-1β and pro-IL-18 to their mature forms IL-1β and IL-18, respectively, and the cell undergoes inflammatory death termed pyroptosis. Here, we reviewed recent findings demonstrating that Brucella abortus ligands activate NLRP3 and AIM2 inflammasomes which lead to control of infection. This protective effect is due to the inflammatory response caused by IL-1β and IL-18 rather than cell death...
July 12, 2016: Seminars in Immunopathology
Chen Qiao, Lin-Xia Zhang, Xi-Yang Sun, Jian-Hua Ding, Ming Lu, Gang Hu
Caspase family has been recognized to be involved in dopaminergic (DA) neuronal death and to exert an unfavorable role in Parkinson's disease (PD) pathology. Our previous study has revealed that caspase-1, as an important component of NLRP3 inflammasome, induces microglia-mediated neuroinflammation in the pathogenesis of PD. However, the role of caspase-1 in DA neuronal degeneration in the onset of PD remains unclear. Here, we showed that caspase-1 knockout ameliorated DA neuronal loss and dyskinesia in 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine/probenecid (MPTP/p)-induced PD model mice...
June 23, 2016: Molecular Neurobiology
Carola J Maturana, Adam Aguirre, Juan C Sáez
Exposure to high levels of glucocorticoids (GCs) during early life induces long-lasting neuroinflammation. GCs induce rapid degranulation of mast cells, which release proinflammatory molecules promoting activation of microglia and astrocytes. The possible involvement of oligodendrocytes, however, remains poorly understood. It was studied whether high GC levels during gestation activates the inflammasome in hippocampal oligodendrocytes of mouse offspring. Oligodendrocytes of control pups showed expression of inflammasome components (NLRP3, ACS, and caspase-1) and their levels were increased by prenatal administration of dexamethasone (DEX), a synthetic GC...
June 17, 2016: Developmental Neurobiology
Alba Jimenez-Pacheco, Miguel Diaz-Hernandez, Marina Arribas-Blázquez, Amaya Sanz-Rodriguez, Luis A Olivos-Oré, Antonio R Artalejo, Mariana Alves, Michael Letavic, M Teresa Miras-Portugal, Ronan M Conroy, Norman Delanty, Michael A Farrell, Donncha F O'Brien, Anindya Bhattacharya, Tobias Engel, David C Henshall
UNLABELLED: Neuroinflammation is thought to contribute to the pathogenesis and maintenance of temporal lobe epilepsy, but the underlying cell and molecular mechanisms are not fully understood. The P2X7 receptor is an ionotropic receptor predominantly expressed on the surface of microglia, although neuronal expression has also been reported. The receptor is activated by the release of ATP from intracellular sources that occurs during neurodegeneration, leading to microglial activation and inflammasome-mediated interleukin 1β release that contributes to neuroinflammation...
June 1, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
Peter M Grace, Keith A Strand, Erika L Galer, Daniel J Urban, Xiaohui Wang, Michael V Baratta, Timothy J Fabisiak, Nathan D Anderson, Kejun Cheng, Lisa I Greene, Debra Berkelhammer, Yingning Zhang, Amanda L Ellis, Hang Hubert Yin, Serge Campeau, Kenner C Rice, Bryan L Roth, Steven F Maier, Linda R Watkins
Opioid use for pain management has dramatically increased, with little assessment of potential pathophysiological consequences for the primary pain condition. Here, a short course of morphine, starting 10 d after injury in male rats, paradoxically and remarkably doubled the duration of chronic constriction injury (CCI)-allodynia, months after morphine ceased. No such effect of opioids on neuropathic pain has previously been reported. Using pharmacologic and genetic approaches, we discovered that the initiation and maintenance of this multimonth prolongation of neuropathic pain was mediated by a previously unidentified mechanism for spinal cord and pain-namely, morphine-induced spinal NOD-like receptor protein 3 (NLRP3) inflammasomes and associated release of interleukin-1β (IL-1β)...
June 14, 2016: Proceedings of the National Academy of Sciences of the United States of America
Ren-Hong Du, Jun Tan, Xi-Yang Sun, Ming Lu, Jian-Hua Ding, Gang Hu
BACKGROUND: Emerging evidence indicates that NLRP3 inflammasome-induced inflammation plays a crucial role in the pathogenesis of depression. Thus, inhibition of NLRP3 inflammasome activation may offer a therapeutic benefit in the treatment of depression. Fluoxetine, a widely used antidepressant, has been shown to have potential antiinflammatory activity, but the underlying mechanisms remain obscure. METHODS: We used a chronic mild stress model and cultured primary macrophage/microglia to investigate the effects of fluoxetine on NLRP3 inflammasome and its underlying mechanisms...
May 11, 2016: International Journal of Neuropsychopharmacology
Yan Zhou, Ming Lu, Ren-Hong Du, Chen Qiao, Chun-Yi Jiang, Ke-Zhong Zhang, Jian-Hua Ding, Gang Hu
BACKGROUND: α-Synuclein (α-Syn), a pathological hallmark of Parkinson's disease (PD), has been recognized to induce the production of interleukin-1β in a process that depends, at least in vitro, on nod-like receptor protein 3 (NLRP3) inflammasome in monocytes. However, the role of NLRP3 inflammasome activation in the onset of PD has not yet been fully established. RESULTS: In this study, we showed that NLRP3 inflammasomes were activated in the serum of PD patients and the midbrain of PD model mice...
2016: Molecular Neurodegeneration
Yuri Kim, Joanne O Davidson, Katherine C Gunn, Anthony R Phillips, Colin R Green, Alistair J Gunn
Neurodegenerative, cardiovascular, and metabolic disorders, once triggered, share a number of common features, including sustained inflammatory cell activation and vascular disruption. These shared pathways are induced independently of any genetic predisposition to the disease or the precise external stimulus. Glial cells respond to injury with an innate immune response that includes release of proinflammatory cytokines and chemokines. Vascular endothelial cells may also be affected, leading to opening of the blood-brain barrier that facilitates invasion by circulating inflammatory cells...
2016: Advances in Protein Chemistry and Structural Biology
Chenhui Li, Jing Wang, Yinquan Fang, Yuan Liu, Tao Chen, Hao Sun, Xin-Fu Zhou, Hong Liao
Inflammation plays an important role in stroke pathology, making it a promising target for stroke intervention. Nafamostat mesilate (NM), a wide-spectrum serine protease inhibitor, is commonly used for treating inflammatory diseases, such as pancreatitis. However, its effect on neuroinflammation after stroke was unknown. Hence, the effects of NM on the inflammatory response post stroke were characterized. After transient middle cerebral artery occlusion (tMCAO) in rats, NM reduced the infarct size, improved behavioral functions, decreased the expression of proinflammatory mediators (TNF-α, IL-1β, iNOS and COX-2) in a time-dependent manner and promoted the expression of different anti-inflammatory factors (CD206, TGF-β, IL-10 and IL-4) at different time points...
August 2016: Brain, Behavior, and Immunity
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