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https://www.readbyqxmd.com/read/28096356/active-mlkl-triggers-the-nlrp3-inflammasome-in-a-cell-intrinsic-manner
#1
Stephanie A Conos, Kaiwen W Chen, Dominic De Nardo, Hideki Hara, Lachlan Whitehead, Gabriel Núñez, Seth L Masters, James M Murphy, Kate Schroder, David L Vaux, Kate E Lawlor, Lisa M Lindqvist, James E Vince
Necroptosis is a physiological cell suicide mechanism initiated by receptor-interacting protein kinase-3 (RIPK3) phosphorylation of mixed-lineage kinase domain-like protein (MLKL), which results in disruption of the plasma membrane. Necroptotic cell lysis, and resultant release of proinflammatory mediators, is thought to cause inflammation in necroptotic disease models. However, we previously showed that MLKL signaling can also promote inflammation by activating the nucleotide-binding oligomerization domain (NOD)-like receptor protein 3 (NLRP3) inflammasome to recruit the adaptor protein apoptosis-associated speck-like protein containing a caspase activation and recruitment domain (ASC) and trigger caspase-1 processing of the proinflammatory cytokine IL-1β...
January 17, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28087651/frontline-science-multiple-cathepsins-promote-inflammasome-independent-particle-induced-cell-death-during-nlrp3-dependent-il-1%C3%AE-activation
#2
Gregory M Orlowski, Shruti Sharma, Jeff D Colbert, Matthew Bogyo, Stephanie A Robertson, Hiroshi Kataoka, Francis K Chan, Kenneth L Rock
Sterile particles cause several chronic, inflammatory diseases, characterized by repeating cycles of particle phagocytosis and inflammatory cell death. Recent studies have proposed that these processes are driven by the NLRP3 inflammasome, a platform activated by phagocytosed particles, which controls both caspase-1-dependent cell death (pyroptosis) and mature IL-1β secretion. After phagocytosis, particles can disrupt lysosomes, and inhibitor studies have suggested that the resulting release of a lysosomal protease-cathepsin B-into the cytosol somehow activates NLRP3...
January 13, 2017: Journal of Leukocyte Biology
https://www.readbyqxmd.com/read/28065854/the-mechanism-of-nlrp3-inflammasome-initiation-trimerization-but-not-dimerization-of-the-nlrp3-pyrin-domain-induces-robust-activation-of-il-1%C3%AE
#3
Petra Sušjan, Samo Roškar, Iva Hafner-Bratkovič
NLRP3 inflammasome is a multiprotein platform for the activation of caspase-1. Despite the increasing number of reports linking NLRP3 inflammasome to a variety of diseases, the mechanism behind the NLRP3 activation remains elusive, especially in terms of the early stages which are critical to the NLRP3 inflammasome assembly. In the present study we aimed to determine the minimal oligomerization state required for the NLRP3 inflammasome activation. For this purpose, NLRP3 pyrin domain (NLRP3(PYD)) was fused to various dimerization and trimerization domains...
January 5, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28062222/absent-in-melanoma-2-proteins-in-sle
#4
REVIEW
Divaker Choubey, Ravichandran Panchanathan
Type I interferons (IFN-α/β)-inducible PYRIN and HIN domain-containing protein family includes Absent in Melanoma 2 (murine Aim2 and human AIM2), murine p202, and human PYRIN-only protein 3 (POP3). The generation of Aim2-deficient mice indicated that the Aim2 protein is essential for inflammasome activation, resulting in the secretion of interleukin-1β (IL-1β) and IL-18 and cell death by pyroptosis. Further, Aim2-deficiency also increased constitutive expression of the IFN-β and expression of the p202 protein...
January 3, 2017: Clinical Immunology: the Official Journal of the Clinical Immunology Society
https://www.readbyqxmd.com/read/28060375/how-ice-lights-the-pyroptosis-fire
#5
Xing Liu, Judy Lieberman
No abstract text is available yet for this article.
January 6, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28045099/cleavage-of-dfna5-by-caspase-3-during-apoptosis-mediates-progression-to-secondary-necrotic-pyroptotic-cell-death
#6
Corey Rogers, Teresa Fernandes-Alnemri, Lindsey Mayes, Diana Alnemri, Gino Cingolani, Emad S Alnemri
Apoptosis is a genetically regulated cell suicide programme mediated by activation of the effector caspases 3, 6 and 7. If apoptotic cells are not scavenged, they progress to a lytic and inflammatory phase called secondary necrosis. The mechanism by which this occurs is unknown. Here we show that caspase-3 cleaves the GSDMD-related protein DFNA5 after Asp270 to generate a necrotic DFNA5-N fragment that targets the plasma membrane to induce secondary necrosis/pyroptosis. Cells that express DFNA5 progress to secondary necrosis, when stimulated with apoptotic triggers such as etoposide or vesicular stomatitis virus infection, but disassemble into small apoptotic bodies when DFNA5 is deleted...
January 3, 2017: Nature Communications
https://www.readbyqxmd.com/read/28018360/atp-induced-inflammasome-activation-and-pyroptosis-is-regulated-by-amp-activated-protein-kinase-in-macrophages
#7
Qing-Bing Zha, Hong-Xia Wei, Chen-Guang Li, Yi-Dan Liang, Li-Hui Xu, Wen-Jing Bai, Hao Pan, Xian-Hui He, Dong-Yun Ouyang
Adenosine triphosphate (ATP) is released by bacteria and host cells during bacterial infection as well as sterile tissue injury, acting as an inducer of inflammasome activation. Previous studies have shown that ATP treatment leads to AMP-activated protein kinase (AMPK) activation. However, it is unclear whether AMPK signaling has been involved in the regulation of ATP-induced inflammasome activation and subsequent pyroptosis. In this study, we aimed to investigate this issue in lipopolysaccharide-activated murine macrophages...
2016: Frontiers in Immunology
https://www.readbyqxmd.com/read/28007731/dying-a-fiery-death-pyroptosis-in-mds
#8
Alison R Walker
No abstract text is available yet for this article.
December 22, 2016: Blood
https://www.readbyqxmd.com/read/28006785/mir-155-is-involved-in-renal-ischemia-reperfusion-injury-via-direct-targeting-of-foxo3a-and-regulating-renal-tubular-cell-pyroptosis
#9
Haoyu Wu, Tao Huang, Liang Ying, Conghui Han, Dawei Li, Yao Xu, Ming Zhang, Shan Mou, Zhen Dong
BACKGROUND/AIMS: Ischemia/reperfusion injury (IRI) plays a crucial role in renal transplantation and can cause renal failure associated with pyroptosis, a pro-inflammatory-induced programmed cell death. Small endogenous non-coding RNAs have been shown to be involved in renal ischemia/reperfusion injury. This study was performed to investigate which miRNAs regulate pyroptosis in response to renal ischemia/reperfusion injury and determine the mechanism underlying this regulation. METHODS: An in vivo rat model of renal IRI was established, and the serum and kidneys were harvested 24 h after reperfusion to assess renal function and histological changes...
2016: Cellular Physiology and Biochemistry
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
#10
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
#11
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
#12
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/27984721/roles-of-caspases-in-necrotic-cell-death
#13
REVIEW
Junying Yuan, Ayaz Najafov, Bénédicte F Py
Caspases were originally identified as important mediators of inflammatory response and apoptosis. Recent discoveries, however, have unveiled their roles in mediating and suppressing two regulated forms of necrotic cell death, termed pyroptosis and necroptosis, respectively. These recent advances have significantly expanded our understanding of the roles of caspases in regulating development, adult homeostasis, and host defense response.
December 15, 2016: Cell
https://www.readbyqxmd.com/read/27980220/berberine-augments-atp-induced-inflammasome-activation-in-macrophages-by-enhancing-ampk-signaling
#14
Chen-Guang Li, Liang Yan, Yan-Yun Jing, Li-Hui Xu, Yi-Dan Liang, Hong-Xia Wei, Bo Hu, Hao Pan, Qing-Bing Zha, Dong-Yun Ouyang, Xian-Hui He
The isoquinoline alkaloid berberine possesses many pharmacological activities including antibacterial infection. Although the direct bactericidal effect of berberine has been documented, its influence on the antibacterial functions of macrophages is largely unknown. As inflammasome activation in macrophages is important for the defense against bacterial infection, we aimed to investigate the influence of berberine on inflammasome activation in murine macrophages. Our results showed that berberine significantly increased ATP-induced inflammasome activation as reflected by enhanced pyroptosis as well as increased release of caspase-1p10 and mature interleukin-1β (IL-1β) in macrophages...
December 12, 2016: Oncotarget
https://www.readbyqxmd.com/read/27974850/hepatitis-c-virus-infection-of-cultured-human-hepatoma-cells-causes-apoptosis-and-pyroptosis-in-both-infected-and-bystander-cells
#15
H M Kofahi, N G A Taylor, K Hirasawa, M D Grant, R S Russell
Individuals infected with hepatitis C virus (HCV) are at high risk of developing progressive liver disease, including cirrhosis and hepatocellular carcinoma (HCC). How HCV infection causes liver destruction has been of significant interest for many years, and apoptosis has been proposed as one operative mechanism. In this study, we employed a tissue culture-adapted strain of HCV (JFH1T) to test effects of HCV infection on induction of programmed cell death (PCD) in Huh-7.5 cells. We found that HCV infection reduced the proliferation rate and induced caspase-3-mediated apoptosis in the infected cell population...
December 15, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27974148/salmonella-induced-inflammasome-activation-in-humans
#16
Damien Bierschenk, Dave Boucher, Kate Schroder
Inflammasomes are macromolecular complexes that assemble upon recognition of pathogen- or danger-associated molecular patterns. Inflammasome assembly is nucleated by the oligomerisation of specific, activated pattern recognition receptors within the cytosol. Inflammasomes function as platforms for the activation of the caspase-1 protease, which in turn triggers the maturation and secretion of the pro-inflammatory cytokines IL-1β and IL-18, and initiates pyroptosis, a highly inflammatory form of lytic cell death...
December 11, 2016: Molecular Immunology
https://www.readbyqxmd.com/read/27964927/long-noncoding-rna-malat1-regulates-renal-tubular-epithelial-pyroptosis-by-modulated-mir-23c-targeting-of-elavl1-in-diabetic-nephropathy
#17
Xue Li, Li Zeng, Chuanwu Cao, Chenhui Lu, Weishuai Lian, Jianhong Han, Xiaojun Zhang, Jing Zhang, Tao Tang, Maoquan Li
Diabetic nephropathy is a common kidney condition in patients with diabetes mellitus, which can result in renal failure. Pyroptosis, the process of pro-inflammatory programmed cell death, plays an important role in the pathogenesis of this disease. Long non-coding RNA MALAT1 has also been shown to be involved in diabetic nephropathy. Here, we investigated the role of MALAT1 and the microRNA miR-23c and its target gene ELAVL1 in renal tubular epithelial cells. Our data demonstrated that MALAT1 expression was substantially increased but miR-23c was decreased in streptozotocin-induced diabetic rats and in high-glucose-treated HK-2 cells...
December 10, 2016: Experimental Cell Research
https://www.readbyqxmd.com/read/27941671/non-canonical-cell-death-induced-by-p53
#18
REVIEW
Atul Ranjan, Tomoo Iwakuma
Programmed cell death is a vital biological process for multicellular organisms to maintain cellular homeostasis, which is regulated in a complex manner. Over the past several years, apart from apoptosis, which is the principal mechanism of caspase-dependent cell death, research on non-apoptotic forms of programmed cell death has gained momentum. p53 is a well characterized tumor suppressor that controls cell proliferation and apoptosis and has also been linked to non-apoptotic, non-canonical cell death mechanisms...
December 9, 2016: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/27941592/pathological-role-and-diagnostic-value-of-endogenous-host-defense-peptides-in-adult-and-neonatal-sepsis-a-systematic-review
#19
Jeffery Ho, Lin Zhang, Xiaodong Liu, Sunny H Wong, Maggie H T Wang, Benson W M Lau, Shirley P C Ngai, Hung Chan, Gordon Choi, Czarina C H Leung, Wai T Wong, Sharon Tsang, Tony Gin, Jun Yu, Matthew T V Chan, William K K Wu
BACKGROUND: Sepsis is a systemic host response to an infection leading to organ failure. This is associated with dynamic expression of endogenous host defense peptides. Dysregulation of these peptides is associated with septic morbidity and mortality. METHODS: We performed a systematic search of articles indexed in Pubmed, ISI Web of Knowledge, EmBase and Scopus database from inception to October 2016. Both preclinical and clinical studies investigating the role of host defense peptides in pathogenesis and as biomarkers for sepsis were included...
December 9, 2016: Shock
https://www.readbyqxmd.com/read/27934691/dead-cert-measuring-cell-death
#20
Lisa C Crowley, Brooke J Marfell, Adrian P Scott, Jeanne A Boughaba, Grace Chojnowski, Melinda E Christensen, Nigel J Waterhouse
Many cells in the body die at specific times to facilitate healthy development or because they have become old, damaged, or infected. Defects in cells that result in their inappropriate survival or untimely death can negatively impact development or contribute to a variety of human pathologies, including cancer, AIDS, autoimmune disorders, and chronic infection. Cell death may also occur following exposure to environmental toxins or cytotoxic chemicals. Although this is often harmful, it can be beneficial in some cases, such as in the treatment of cancer...
December 1, 2016: Cold Spring Harbor Protocols
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