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https://www.readbyqxmd.com/read/28204973/iaps-and-cell-death
#1
John Silke, James Vince
IAPs were named as inhibitors of apoptosis, programmed cell death, but it has become apparent that they are regulators of other types of cell death too. Because they inhibit cell death in cancer cells there has been an intense interest in developing inhibitors of these proteins to induce or sensitise cancer cells to death. In this article, we will discuss the involvement of IAPs in the apoptosis, necroptosis and pyroptosis programmed cell death paradigms. All these types of cell death are intimately involved with causing or repressing inflammation and it should perhaps therefore come as no surprise that IAPs are also involved in regulating inflammation directly...
February 16, 2017: Current Topics in Microbiology and Immunology
https://www.readbyqxmd.com/read/28197335/caspase-8-not-so-silently-deadly
#2
REVIEW
Rebecca Feltham, James E Vince, Kate E Lawlor
Apoptosis is a caspase-dependent programmed form of cell death, which is commonly believed to be an immunologically silent process, required for mammalian development and maintenance of cellular homoeostasis. In contrast, lytic forms of cell death, such as RIPK3- and MLKL-driven necroptosis, and caspase-1/11-dependent pyroptosis, are postulated to be inflammatory via the release of damage associated molecular patterns (DAMPs). Recently, the function of apoptotic caspase-8 has been extended to the negative regulation of necroptosis, the cleavage of inflammatory interleukin-1β (IL-1β) to its mature bioactive form, either directly or via the NLRP3 inflammasome, and the regulation of cytokine transcriptional responses...
January 2017: Clinical & Translational Immunology
https://www.readbyqxmd.com/read/28196749/recent-insights-into-the-molecular-mechanisms-underlying-pyroptosis-and-gasdermin-family-functions
#3
REVIEW
Robin A Aglietti, Erin C Dueber
Pyroptosis is an inflammatory form of cell death that not only protects multicellular organisms from invading pathogenic bacteria and microbial infections, but can also lead to sepsis and lethal septic shock if overactivated. Here, we present an overview of recent developments within the pyroptosis field, beginning with the discovery of Gasdermin D (GSDMD) as a substrate of caspase-1 and caspase-11 upon detection of cytosolic lipopolysaccharide (LPS). Cleavage releases the N-terminal domain of GSDMD, causing it to form cytotoxic pores in the plasma membrane of cells...
February 11, 2017: Trends in Immunology
https://www.readbyqxmd.com/read/28192059/inflammasomes-key-mediators-of-lung-immunity
#4
Judie A Howrylak, Kiichi Nakahira
Inflammasomes are key inflammatory signaling platforms that detect microbial substances, sterile environmental insults, and molecules derived from host cells. Activation of the inflammasome promotes caspase-1-mediated secretion of proinflammatory cytokines interleukin (IL)-1β and IL-18 and pyroptosis. Recent developments in this field demonstrate the crucial role of the inflammasome in a wide range of disease models. Although inflammasomes are a crucial part of host defense mechanisms against pathogens, the exuberant immune response resulting from inflammasome activation also contributes to the development of various diseases...
February 10, 2017: Annual Review of Physiology
https://www.readbyqxmd.com/read/28174728/necrosis-apoptosis-necroptosis-pyroptosis-it-matters-how-acinar-cells-die-during-pancreatitis
#5
EDITORIAL
Matthias Sendler, Julia Mayerle, Markus M Lerch
No abstract text is available yet for this article.
July 2016: Cellular and Molecular Gastroenterology and Hepatology
https://www.readbyqxmd.com/read/28154144/gene-polymorphism-linked-to-increased-asthma-and-ibd-risk-alters-gasdermin-b-structure-a-sulfatide-and-phosphoinositide-binding-protein
#6
Kinlin L Chao, Liudmila Kulakova, Osnat Herzberg
The exact function of human gasdermin-B (GSDMB), which regulates differentiation and growth of epithelial cells, is yet to be elucidated. In human epidermal growth factor receptor 2 (HER2)-positive breast cancer, GSDMB gene amplification and protein overexpression indicate a poor response to HER2-targeted therapy. Genome-wide association studies revealed a correlation between GSDMB SNPs and an increased susceptibility to Crohn's disease, ulcerative colitis, and asthma. The N- and C-terminal domains of all gasdermins possess lipid-binding and regulatory activities, respectively...
February 1, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28151471/nlrp3-inflammasome-activation-mediates-radiation-induced-pyroptosis-in-bone-marrow-derived-macrophages
#7
Yan-Gang Liu, Ji-Kuai Chen, Zi-Teng Zhang, Xiu-Juan Ma, Yong-Chun Chen, Xiu-Ming Du, Hong Liu, Ying Zong, Guo-Cai Lu
A limit to the clinical benefit of radiotherapy is not an incapacity to eliminate tumor cells but rather a limit on its capacity to do so without destroying normal tissue and inducing inflammation. Recent evidence reveals that the inflammasome is essential for mediating radiation-induced cell and tissue damage. In this study, using primary cultured bone marrow-derived macrophages (BMDM) and a mouse radiation model, we explored the role of NLRP3 inflammasome activation and the secondary pyroptosis underlying radiation-induced immune cell death...
February 2, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28147281/the-atypical-ubiquitin-e2-conjugase-ube2l3-is-an-indirect-caspase-1-target-and-controls-il-1%C3%AE-secretion-by-inflammasomes
#8
Matthew J G Eldridge, Julia Sanchez-Garrido, Gil Ferreira Hoben, Philippa J Goddard, Avinash R Shenoy
Caspase-1 activation by inflammasome signaling scaffolds initiates inflammation and antimicrobial responses. Caspase-1 proteolytically converts newly induced pro-interleukin 1 beta (IL-1β) into its mature form and directs its secretion, triggering pyroptosis and release of non-substrate alarmins such as interleukin 1 alpha (IL-1α) and HMGB1. While some caspase-1 substrates involved in these events are known, the identities and roles of non-proteolytic targets remain unknown. Here, we use unbiased proteomics to show that the UBE2L3 ubiquitin conjugase is an indirect target of caspase-1...
January 31, 2017: Cell Reports
https://www.readbyqxmd.com/read/28140444/the-nlrp3-inflammasome-contributes-to-host-protection-during-sporothrix-schenckii-infection
#9
Amanda Costa Gonçalves, Lucas Souza Ferreira, Francine Alessandra Manente, Carolina Maria Quinello Gomes de Faria, Marisa Campos Polesi, Cleverton Roberto de Andrade, Dario Simões Zamboni, Iracilda Zeppone Carlos
Sporotrichosis is a mycosis caused by fungi from the Sporothrix schenckii species complex, whose prototypical member is Sporothrix schenckii sensu stricto. Pattern recognition receptors (PRRs) recognize and respond to pathogen-associated molecular patterns (PAMPs) and shape the following adaptive immune response. A family of PRRs most frequently associated with fungal recognition is the nucleotide-binding oligomerization domain-like receptor (NLR). After PAMP recognition, NLR family pyrin domain-containing 3 (NLRP3) binds to apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) and caspase-1 to form the NLRP3 inflammasome...
January 31, 2017: Immunology
https://www.readbyqxmd.com/read/28138860/preferential-pattern-of-mouse-neutrophil-cell-death-in-response-to-various-stimulants
#10
Nuttira Luehong, Juthamart Khaowmek, Kanruethai Wongsawan, Phongsakorn Chuammitri
Neutrophils undergo cell death processes once their physiological function has been fulfilled. Apoptosis, necrosis, pyroptosis, or NETosis, a unique form of cell death, could occur, depending on the type of stimulant or inhibitory intervention. We investigated whether phorbol myristate acetate (PMA) and Klebsiella pneumoniae (KP), serving as stimulants, or whether an inhibitor (cytochalasin B, CytB) could alter the morphology and gene expression pattern associated with mouse neutrophil cell death. Fluorescence microscopy, flow cytometry, and real-time PCR approaches were used to identify morphological changes, percentages of cell death, and gene expression patterns, respectively...
January 30, 2017: In Vitro Cellular & Developmental Biology. Animal
https://www.readbyqxmd.com/read/28138137/programmed-cell-death-as-a-defence-against-infection
#11
REVIEW
Ine Jorgensen, Manira Rayamajhi, Edward A Miao
Eukaryotic cells can die from physical trauma, which results in necrosis. Alternatively, they can die through programmed cell death upon the stimulation of specific signalling pathways. In this Review, we discuss the role of different cell death pathways in innate immune defence against bacterial and viral infection: apoptosis, necroptosis, pyroptosis and NETosis. We describe the interactions that interweave different programmed cell death pathways, which create complex signalling networks that cross-guard each other in the evolutionary 'arms race' with pathogens...
January 31, 2017: Nature Reviews. Immunology
https://www.readbyqxmd.com/read/28129896/inflammasomes-in-the-lung
#12
James W Pinkerton, Richard Y Kim, Avril A B Robertson, Jeremy A Hirota, Lisa G Wood, Darryl A Knight, Matthew A Cooper, Luke A J O'Neill, Jay C Horvat, Philip M Hansbro
Innate immune responses act as first line defences upon exposure to potentially noxious stimuli. The innate immune system has evolved numerous intracellular and extracellular receptors that undertake surveillance for potentially damaging particulates. Inflammasomes are intracellular innate immune multiprotein complexes that form and are activated following interaction with these stimuli. Inflammasome activation leads to the cleavage of pro-IL-1β and release of the pro-inflammatory cytokine, IL-1β, which initiates acute phase pro-inflammatory responses, and other responses are also involved (IL-18, pyroptosis)...
January 24, 2017: Molecular Immunology
https://www.readbyqxmd.com/read/28129545/snapshot-the-noncanonical-inflammasome
#13
Jingjin Ding, Feng Shao
This SnapShot depicts how the noncanonical inflammasome pathway is initiated and activated, as well as its effector mechanism in triggering pyroptosis and immune defenses.
January 26, 2017: Cell
https://www.readbyqxmd.com/read/28109721/inflammasome-priming-in-sterile-inflammatory-disease
#14
REVIEW
Meghana N Patel, Richard G Carroll, Silvia Galván-Peña, Evanna L Mills, Robin Olden, Martha Triantafilou, Amaya I Wolf, Clare E Bryant, Kathy Triantafilou, Seth L Masters
The inflammasome is a cytoplasmic protein complex that processes interleukins (IL)-1β and IL-18, and drives a form of cell death known as pyroptosis. Oligomerization of this complex is actually the second step of activation, and a priming step must occur first. This involves transcriptional upregulation of pro-IL-1β, inflammasome sensor NLRP3, or the non-canonical inflammasome sensor caspase-11. An additional aspect of priming is the post-translational modification of particular inflammasome constituents...
January 18, 2017: Trends in Molecular Medicine
https://www.readbyqxmd.com/read/28096356/active-mlkl-triggers-the-nlrp3-inflammasome-in-a-cell-intrinsic-manner
#15
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...
February 7, 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
#16
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
#17
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
#18
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
#19
Xing Liu, Judy Lieberman
No abstract text is available yet for this article.
February 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
#20
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
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