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Inflammasome phosphorylation

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https://www.readbyqxmd.com/read/27882934/macrophage-dependent-il-1%C3%AE-production-induces-cardiac-arrhythmias-in-diabetic-mice
#1
Gustavo Monnerat, Micaela L Alarcón, Luiz R Vasconcellos, Camila Hochman-Mendez, Guilherme Brasil, Rosana A Bassani, Oscar Casis, Daniela Malan, Leonardo H Travassos, Marisa Sepúlveda, Juan Ignacio Burgos, Martin Vila-Petroff, Fabiano F Dutra, Marcelo T Bozza, Claudia N Paiva, Adriana Bastos Carvalho, Adriana Bonomo, Bernd K Fleischmann, Antonio Carlos Campos de Carvalho, Emiliano Medei
Diabetes mellitus (DM) encompasses a multitude of secondary disorders, including heart disease. One of the most frequent and potentially life threatening disorders of DM-induced heart disease is ventricular tachycardia (VT). Here we show that toll-like receptor 2 (TLR2) and NLRP3 inflammasome activation in cardiac macrophages mediate the production of IL-1β in DM mice. IL-1β causes prolongation of the action potential duration, induces a decrease in potassium current and an increase in calcium sparks in cardiomyocytes, which are changes that underlie arrhythmia propensity...
November 24, 2016: Nature Communications
https://www.readbyqxmd.com/read/27870591/human-transcriptome-response-to-immunization-with-live-attenuated-venezuelan-equine-encephalitis-virus-vaccine-tc-83-analysis-of-whole-blood
#2
Rebecca A Erwin-Cohen, Aimee I Porter, Phillip R Pittman, Cynthia A Rossi, Luis DaSilva
Venezuelan equine encephalitis virus (VEEV) is an important human and animal alphavirus pathogen transmitted by mosquitoes. The virus is endemic in Central and South America, but has also caused equine outbreaks in southwestern areas of the United States. In an effort to better understand the molecular mechanisms of the development of immunity to this important pathogen, we performed transcriptional analysis from whole, unfractionated human blood of patients who had been immunized with the live-attenuated vaccine strain of VEEV, TC-83...
November 21, 2016: Human Vaccines & Immunotherapeutics
https://www.readbyqxmd.com/read/27859049/lps-primed-heterotolerant-dendritic-cells-suppress-experimental-autoimmune-uveoretintitis-by-multiple-mechanisms
#3
Izabela P Klaska, Elizabeth Muckersie, Cristina Martin-Granados, Maria Christofi, John V Forrester
Exposure of bone marrow derived dendritic cells (BMDC) to high dose ultrapure lipopolysaccharide for 24 hours (h) (LPS-primed BMDC) enhances their potency in preventing inter-photoreceptor retinoid binding protein (IRBP): complete Freund's adjuvant (CFA)-induced experimental autoimmune uveoretinitis (EAU). LPS-primed BMDC are refractory to further exposure to LPS (= endotoxin tolerance, ET), evidenced here by decreased phosphorylation of TANK-binding kinase 1 (TBK1), interferon regulatory factor 3 (IRF3), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (p38 MAPK) as well as impaired nuclear translocation of nuclear factor κB (NF-κB) and IRF3, resulting in reduced tumor necrosis factor alpha (TNF-α), interleukin (IL)-6, IL-12 and interferon beta (IFN-β) secretion...
November 15, 2016: Immunology
https://www.readbyqxmd.com/read/27806131/the-listeria-monocytogenes-pasta-kinase-prka-and-its-substrate-yvck-are-required-for-cell-wall-homeostasis-metabolism-and-virulence
#4
Daniel A Pensinger, Kyle M Boldon, Grischa Y Chen, William J B Vincent, Kyle Sherman, Meng Xiong, Adam J Schaenzer, Emily R Forster, Jörn Coers, Rob Striker, John-Demian Sauer
Obstacles to bacterial survival and replication in the cytosol of host cells, and the mechanisms used by bacterial pathogens to adapt to this niche are not well understood. Listeria monocytogenes is a well-studied Gram-positive foodborne pathogen that has evolved to invade and replicate within the host cell cytosol; yet the mechanisms by which it senses and responds to stress to survive in the cytosol are largely unknown. To assess the role of the L. monocytogenes penicillin-binding-protein and serine/threonine associated (PASTA) kinase PrkA in stress responses, cytosolic survival and virulence, we constructed a ΔprkA deletion mutant...
November 2016: PLoS Pathogens
https://www.readbyqxmd.com/read/27796369/pyk2-activates-the-nlrp3-inflammasome-by-directly-phosphorylating-asc-and-contributes-to-inflammasome-dependent-peritonitis
#5
I-Che Chung, Chun-Nan OuYang, Sheng-Ning Yuan, Hsin-Pai Li, Jeng-Ting Chen, Hui-Ru Shieh, Yu-Jen Chen, David M Ojcius, Ching-Liang Chu, Jau-Song Yu, Yu-Sun Chang, Lih-Chyang Chen
The inflammasome adaptor protein, ASC, contributes to both innate immune responses and inflammatory diseases via self-oligomerization, which leads to the activation of the protease, caspase-1. Here, we report that the cytosolic tyrosine kinases, FAK and Pyk2, are differentially involved in NLRP3 and AIM2 inflammasome activation. The inhibition of FAK and Pyk2 with RNA interference or chemical inhibitors dramatically abolished ASC oligomerization, caspase-1 activation, and IL-1β secretion in response to NLRP3 or AIM2 stimulation...
October 31, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27784694/deficiency-of-mpges-1-exacerbates-renal-fibrosis-and-inflammation-in-mice-with-unilateral-ureteral-obstruction
#6
Renfei Luo, Yutaka Kakizoe, Feifei Wang, Xiang Fan, Shan Hu, Tianxin Yang, Weidong Wang, Chunling Li
Microsomal prostaglandin E2 synthase-1 (mPGES-1), an inducible enzyme that converts prostaglandin H2 to prostaglandin E2 (PGE2), plays an important role in a variety of inflammatory diseases. We investigated the contribution of mPGES-1 to renal fibrosis and inflammation in unilateral ureteral obstruction (UUO) for 7 days using wild type (WT) and mPGES-1 knockout (KO) mice. UUO induced increased mRNA and protein expression of mPGES-1 and cyclooxygenase-2 in WT mice. UUO was associated with increased renal PGE2 content and upregulated PGE2 receptor (EP) 4 expression in obstructed kidneys of both WT and KO mice; EP4 expression levels were higher in KO mice with UUO than that in WT mice...
October 26, 2016: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/27779186/pkm2-dependent-glycolysis-promotes-nlrp3-and-aim2-inflammasome-activation
#7
Min Xie, Yan Yu, Rui Kang, Shan Zhu, Liangchun Yang, Ling Zeng, Xiaofang Sun, Minghua Yang, Timothy R Billiar, Haichao Wang, Lizhi Cao, Jianxin Jiang, Daolin Tang
Sepsis, severe sepsis and septic shock are the main cause of mortality in non-cardiac intensive care units. Immunometabolism has been linked to sepsis; however, the precise mechanism by which metabolic reprogramming regulates the inflammatory response is unclear. Here we show that aerobic glycolysis contributes to sepsis by modulating inflammasome activation in macrophages. PKM2-mediated glycolysis promotes inflammasome activation by modulating EIF2AK2 phosphorylation in macrophages. Pharmacological and genetic inhibition of PKM2 or EIF2AK2 attenuates NLRP3 and AIM2 inflammasomes activation, and consequently suppresses the release of IL-1β, IL-18 and HMGB1 by macrophages...
October 25, 2016: Nature Communications
https://www.readbyqxmd.com/read/27777559/curcumin-represses-nlrp3-inflammasome-activation-via-tlr4-myd88-nf-%C3%AE%C2%BAb-and-p2x7r-signaling-in-pma-induced-macrophages
#8
Fanqi Kong, Bozhi Ye, Jiatian Cao, Xueli Cai, Lu Lin, Shanjun Huang, Weijian Huang, Zhouqing Huang
Aims: In the NOD-like receptor (NLR) family, the pyrin domain containing 3 (NLRP3) inflammasome is closely related to the progression of atherosclerosis. This study aimed to assess the effects of curcumin on NLRP3 inflammasome in phorbol 12-myristate 13-acetate (PMA)-induced macrophages and explore its underlying mechanism. Methods: Human monocytic THP-1 cells were pretreated with curcumin for 1 h and subsequently induced with PMA for 48 h. Total protein was collected for Western blot analysis. Cytokine interleukin (IL)-1β release and nuclear factor kappa B (NF-κB) p65 translocation were detected by ELISA assay and cellular NF-κB translocation kit, respectively...
2016: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/27769021/the-neuroprotection-of-sinomenine-against-ischemic-stroke-in-mice-by-suppressing-nlrp3-inflammasome-via-ampk-signaling
#9
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...
November 2016: International Immunopharmacology
https://www.readbyqxmd.com/read/27764250/histone-h2b-ifi16-recognition-of-nuclear-herpesviral-genome-induces-cytoplasmic-interferon-%C3%AE-responses
#10
Jawed Iqbal, Mairaj Ahmed Ansari, Binod Kumar, Dipanjan Dutta, Arunava Roy, Leela Chikoti, Gina Pisano, Sujoy Dutta, Shahrooz Vahedi, Mohanan Valiya Veettil, Bala Chandran
IFI16 (gamma-interferon-inducible protein 16), a predominantly nuclear protein involved in transcriptional regulation, also functions as an innate immune response DNA sensor and induces the IL-1β and antiviral type-1 interferon-β (IFN-β) cytokines. We have shown that IFI16, in association with BRCA1, functions as a sequence independent nuclear sensor of episomal dsDNA genomes of KSHV, EBV and HSV-1. Recognition of these herpesvirus genomes resulted in IFI16 acetylation, BRCA1-IFI16-ASC-procaspase-1 inflammasome formation, cytoplasmic translocation, and IL-1β generation...
October 2016: PLoS Pathogens
https://www.readbyqxmd.com/read/27751938/friedelane-type-triterpenoids-as-selective-anti-inflammatory-agents-by-regulation-of-differential-signaling-pathways-in-lps-stimulated-macrophages
#11
Andrea Villar-Lorenzo, Alejandro E Ardiles, Ana I Arroba, Enrique Hernández-Jiménez, Virginia Pardo, Eduardo López-Collazo, Ignacio A Jiménez, Isabel L Bazzocchi, Águeda González-Rodríguez, Ángela M Valverde
A series of 31 pentacyclic triterpenoids isolated from the root barks of Celastrus vulcanicola and Maytenus jelskii were tested for cytotoxicity and inhibitory activity against lipopolysaccharide (LPS)-induced nitric oxide (NO) production in RAW 264.7 macrophages. Compounds 18 (C18) and 25 (C25) exhibited significant inhibition of LPS-induced NO release at 50 and 25μM concentrations, respectively, and decreased mRNAs of pro-inflammatory cytokines. At the molecular level, C18 neither inhibited LPS-mediated phosphorylation of mitogen activated protein kinases (MAPKs) nor nuclear translocation of nuclear factor kappa beta (NFκB)...
December 15, 2016: Toxicology and Applied Pharmacology
https://www.readbyqxmd.com/read/27746687/ginsenoside-rb1-and-compound-k-improve-insulin-signaling-and-inhibit-er-stress-associated-nlrp3-inflammasome-activation-in-adipose-tissue
#12
Weijie Chen, Junlian Wang, Yong Luo, Tao Wang, Xiaochun Li, Aiyun Li, Jia Li, Kang Liu, Baolin Liu
BACKGROUND: This study was designed to investigate whether ginsenoside Rb1 (Rb1) and compound K (CK) ameliorated insulin resistance by suppressing endoplasmic reticulum (ER) stress-induced inflammation in adipose tissue. METHODS: To induce ER stress, epididymal adipose tissue from mice or differentiated 3T3 adipocytes were exposed to high glucose. The effects of Rb1 and CK on reactive oxygen species production, ER stress, TXNIP/NLRP3 inflammasome activation, inflammation, insulin signaling activation, and glucose uptake were detected by western blot, emzyme-linked immunosorbent assay, or fluorometry...
October 2016: Journal of Ginseng Research
https://www.readbyqxmd.com/read/27733681/vitamin-b6-prevents-il-1%C3%AE-production-by-inhibiting-nlrp3-inflammasome-activation
#13
Peipei Zhang, Kohsuke Tsuchiya, Takeshi Kinoshita, Hiroko Kushiyama, Sofya Suidasari, Mizuki Hatakeyama, Hisanori Imura, Norihisa Kato, Takashi Suda
Vitamin B6 includes six water-soluble vitamers: pyridoxal (PL), pyridoxamine (PM), pyridoxine (PN), and their phosphorylated forms. Pyridoxal 5'-phosphate (PLP) is an important cofactor for many metabolic enzymes. Several lines of evidence demonstrate that blood levels of PLP are significantly lower in patients with inflammation than in control subjects, and that vitamin B6 has anti-inflammatory effects, with therapeutic potential for a variety of inflammatory diseases. Although one of our group (NK) previously demonstrated that PL inhibits the NF-κB pathway, the molecular mechanism by which vitamin B6 suppresses inflammation is not well understood...
October 12, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27694988/monosodium-urate-crystal-induced-pro-interleukin-1%C3%AE-production-is-post-transcriptionally-regulated-via-the-p38-signaling-pathway-in-human-monocytes
#14
Yeon-Ho Chung, Dong-Hyun Kim, Won-Woo Lee
IL-1β is a key mediator of sterile inflammation in response to endogenous particulates, a type of damage-associated molecular pattern (DAMPs) molecule derived from damaged cells. Despite the well-known role of sterile particulates such as monosodium urate (MSU) crystals as inflammasome inducers in monocytes/macrophages, little is known regarding how pro-IL-1β synthesis is induced under sterile inflammatory conditions. We provide evidence that MSU crystals post-transcriptionally induce the rapid production of pro-IL-1β in human primary monocytes...
October 3, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27692610/bile-acids-control-inflammation-and-metabolic-disorder-through-inhibition-of-nlrp3-inflammasome
#15
Chuansheng Guo, Shujun Xie, Zhexu Chi, Jinhua Zhang, Yangyang Liu, Li Zhang, Mingzhu Zheng, Xue Zhang, Dajing Xia, Yuehai Ke, Linrong Lu, Di Wang
Reciprocal interactions between the metabolic system and immune cells play pivotal roles in diverse inflammatory diseases, but the underlying mechanisms remain elusive. The activation of bile acid-mediated signaling has been linked to improvement in metabolic syndromes and enhanced control of inflammation. Here, we demonstrated that bile acids inhibited NLRP3 inflammasome activation via the TGR5-cAMP-PKA axis. TGR5 bile acid receptor-induced PKA kinase activation led to the ubiquitination of NLRP3, which was associated with the PKA-induced phosphorylation of NLRP3 on a single residue, Ser 291...
October 18, 2016: Immunity
https://www.readbyqxmd.com/read/27569559/the-yersinia-virulence-factor-yopm-hijacks-host-kinases-to-inhibit-type-iii-effector-triggered-activation-of-the-pyrin-inflammasome
#16
Lawton K Chung, Yong Hwan Park, Yueting Zheng, Igor E Brodsky, Patrick Hearing, Daniel L Kastner, Jae Jin Chae, James B Bliska
Pathogenic Yersinia, including Y. pestis, the agent of plague in humans, and Y. pseudotuberculosis, the related enteric pathogen, deliver virulence effectors into host cells via a prototypical type III secretion system to promote pathogenesis. These effectors, termed Yersinia outer proteins (Yops), modulate multiple host signaling responses. Studies in Y. pestis and Y. pseudotuberculosis have shown that YopM suppresses infection-induced inflammasome activation; however, the underlying molecular mechanism is largely unknown...
September 14, 2016: Cell Host & Microbe
https://www.readbyqxmd.com/read/27548431/nlrp3-inflammasome-inhibition-is-disrupted-in-a-group-of-auto-inflammatory-disease-caps-mutations
#17
Leanne Mortimer, France Moreau, Justin A MacDonald, Kris Chadee
Inflammasomes are positioned to rapidly escalate the intensity of inflammation by activating interleukin (IL)-1β, IL-18 and cell death by pyroptosis. However, negative regulation of inflammasomes remains poorly understood, as is the signaling cascade that dampens inflammasome activity. We found that rapid NLRP3 inflammasome activation was directly inhibited by protein kinase A (PKA), which was induced by prostaglandin E2 (PGE2) signaling via the PGE2 receptor E-prostanoid 4 (EP4). PKA directly phosphorylated the cytoplasmic receptor NLRP3 and attenuated its ATPase function...
October 2016: Nature Immunology
https://www.readbyqxmd.com/read/27509390/double-stranded-rna-interacts-with-toll-like-receptor-3-in-driving-the-acute-inflammatory-response-following-lung-contusion
#18
Madathilparambil V Suresh, Bivin Thomas, David Machado-Aranda, Vladislov A Dolgachev, Sadeesh Kumar Ramakrishnan, Nicholas Talarico, Karen Cavassani, Matthew A Sherman, Mark R Hemmila, Steven L Kunkel, Nils G Walter, Cory M Hogaboam, Krishnan Raghavendran
OBJECTIVES: Lung contusion is a major risk factor for the development of acute respiratory distress syndrome. We set to determine the role of toll-like receptor 3 and the binding of double-stranded RNA in the pathogenesis of sterile injury following lung contusion. DESIGN: Toll-like receptor 3 expression was analyzed in postmortem lung samples from patients with lung contusion. Unilateral lung contusion was induced in toll-like receptor 3 (-/-), TIR-domain-containing adapter-inducing interferon-β (-/-), and wild-type mice...
November 2016: Critical Care Medicine
https://www.readbyqxmd.com/read/27475900/toxoplasma-gondii-mitogen-activated-protein-kinases-are-associated-with-inflammasome-activation-in-infected-mice
#19
Shuchao Wang, Zedong Wang, Yi Gu, Zhongyu Li, Zhongyuan Li, Feng Wei, Quan Liu
Toxoplasma gondii can activate the nucleotide-binding domain and leucine-rich repeat-containing proteins NLRP1/3 inflammasomes, which mediate host resistance to the infection. Here we showed that deletion of mitogen-activated protein kinases MAPK1 and MAPK2 of type I parasite decreases acute virulence in mice, characterized by low levels of interleukin (IL)-18, NLRP1/3, ASC, and caspase-1, and high levels of IL-10 and interferon (IFN)-β transcripts. Additionally, the mutants increased phosphorylation of STAT1, and decreased phosphorylation of STAT3...
July 27, 2016: Microbes and Infection
https://www.readbyqxmd.com/read/27474884/the-myeloid-heat-shock-transcription-factor-1-%C3%AE-catenin-axis-regulates-nlr-family-pyrin-domain-containing-3-inflammasome-activation-in-mouse-liver-ischemia-reperfusion-injury
#20
Shi Yue, Jianjun Zhu, Ming Zhang, Changyong Li, Xingliang Zhou, Min Zhou, Michael Ke, Ronald W Busuttil, Qi-Long Ying, Jerzy W Kupiec-Weglinski, Qiang Xia, Bibo Ke
: Heat shock transcription factor 1 (HSF1) has been implicated in the differential regulation of cell stress and disease states. β-catenin activation is essential for immune homeostasis. However, little is known about the role of macrophage HSF1-β-catenin signaling in the regulation of NLRP3 inflammasome activation during ischemia/reperfusion (I/R) injury (IRI) in the liver. This study investigated the functions and molecular mechanisms by which HSF1-β-catenin signaling influenced NLRP3-mediated innate immune response in vivo and in vitro...
November 2016: Hepatology: Official Journal of the American Association for the Study of Liver Diseases
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