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Journal articles on the topic 'Inflammasom'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 February 2022

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1

Uchima, Miki, and Eicke Latz. "Inflammasom Signaling und chronische Entzündungsreaktionen." Trillium Immunologie 5, no. 1 (2021): 54–60. http://dx.doi.org/10.47184/ti.2021.01.06.

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Inflammasome sind Multiproteinkomplexe, die typischerweise aus drei Proteinentitäten – einem Sensor, einem Adaptor und Caspase 1 – bestehen. Sie werden als Antwort auf die Erkennung von Pathogen-assoziierten molekularen Strukturen (PAMPs) oder Gefahren-assoziierten molekularen Strukturen (DAMPs) gebildet. Eine Schlüsselrolle im Inflammasom-Signalweg spielt dabei das Zymogen Pro-Caspase 1, das zunächst selbst durch Autoprozessierung aktiviert werden muss. Aktive Caspase 1 prozessiert die Vorstufen der pro-inflammatorischen Interleukine (IL) IL-1beta (IL-1β) und IL-18, die daraufhin sekretiert w

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2

Aringer, M., C. Hedrich, and A. K. Tausche. "Inflammasom und Gicht." Zeitschrift für Rheumatologie 75, no. 6 (2016): 537–41. http://dx.doi.org/10.1007/s00393-016-0131-1.

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3

Cordero, Mario D., and Jesús Ruiz-Cabello. "Inflamm-ageing or inflammasom-ageing as independent events." Aging 12, no. 18 (2020): 17759–60. http://dx.doi.org/10.18632/aging.104108.

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4

Hofmann, S. R., N. Bruck, G. Hahn, A. Rösen-Wolff, and C. M. Hedrich. "Systemisch inflammatorische Erkrankungen als Differenzialdiagnose in der Neugeborenenperiode – Inflammasom-vermittelte Erkrankungen." Arthritis und Rheuma 38, no. 02 (2018): 125–31. http://dx.doi.org/10.1055/s-0038-1649292.

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ZusammenfassungAutoinflammatorische Erkrankungen sind durch systemische oder organbezogene Entzündung gekennzeichnet, welche zumindest initial von fehlregulierten Mechanismen des angeborenen Immunsystems ausgehen. Einige monogene autoinflammatorische Erkrankungen manifestieren in der Perinatalperiode, sodass sie Differenzialdiagnosen zu Infektionen des Neugeborenen darstellen. Im vorliegenden Artikel werden Einblicke in die klinische Präsentation und die molekulare Pathophysiologie Inflammasom-vermittelter monogener Erkrankungen mit Manifestation im Neugeborenenalter gegeben.

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5

Manigold, Tobias. "Ursachen, Mechanismen und mögliche therapeutische Ziele der Gicht." Therapeutische Umschau 73, no. 3 (2016): 147–52. http://dx.doi.org/10.1024/0040-5930/a000771.

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Zusammenfassung. Die Gicht ist die häufigste Arthritis weltweit mit zunehmender Prävalenz in den entwickelten Ländern und mit enormen sozioökonomischen Konsequenzen. Das Wissen über die Pathomechanismen, welche zur Arthritis führen und diese einschränken, hat in den letzten Jahren stark zugenommen. Entsprechend zeichnen sich auch neue Therapieansätze und Therapeutika ab. In dieser Übersichtsarbeit werden neben einigen Aspekten der Klinik, Diagnose und Therapie der Gicht, detailliert die intrazellulären Mechanismen, welche zur NLRP3 Inflammasom Aktivierung und IL-1beta Sekretion führen, behande

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6

Inoue, Makoto, and Mari L. Shinohara. "NLRP3 Inflammasome and MS/EAE." Autoimmune Diseases 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/859145.

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Inflammasomes are cytosolic sensors that detect pathogens and danger signals in the innate immune system. The NLRP3 inflammasome is currently the most fully characterized inflammasome and is known to detect a wide array of microbes and endogenous damage-associated molecules. Possible involvement of the NLRP3 inflammasome (or inflammasomes) in the development of multiple sclerosis (MS) was suggested in a number of studies. Recent studies showed that the NLRP3 inflammasome exacerbates experimental autoimmune encephalomyelitis (EAE), an animal model of MS, although EAE can also develop without th

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7

Wagatsuma, Kohei, and Hiroshi Nakase. "Contradictory Effects of NLRP3 Inflammasome Regulatory Mechanisms in Colitis." International Journal of Molecular Sciences 21, no. 21 (2020): 8145. http://dx.doi.org/10.3390/ijms21218145.

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The inflammasome is an intracellular molecular complex, which is mainly involved in innate immunity. Inflammasomes are formed in response to danger signals, associated with infection and injury, and mainly regulate the secretion of interleukin-1β and interleukin-18. Inflammasome dysregulation is known to be associated with various diseases and conditions, and its regulatory mechanisms have become of great interest in recent years. In the colon, inflammasomes have been reported to be associated with autophagy and the microbiota, and their dysregulation contributes to colitis and. However, the d

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8

Spalinger, Marianne R., Marlene Schwarzfischer, and Michael Scharl. "The Role of Protein Tyrosine Phosphatases in Inflammasome Activation." International Journal of Molecular Sciences 21, no. 15 (2020): 5481. http://dx.doi.org/10.3390/ijms21155481.

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Inflammasomes are multi-protein complexes that mediate the activation and secretion of the inflammatory cytokines IL-1β and IL-18. More than half a decade ago, it has been shown that the inflammasome adaptor molecule, ASC requires tyrosine phosphorylation to allow effective inflammasome assembly and sustained IL-1β/IL-18 release. This finding provided evidence that the tyrosine phosphorylation status of inflammasome components affects inflammasome assembly and that inflammasomes are subjected to regulation via kinases and phosphatases. In the subsequent years, it was reported that activation o

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9

Forn-Cuní, Gabriel, Annemarie H. Meijer, and Monica Varela. "Zebrafish in Inflammasome Research." Cells 8, no. 8 (2019): 901. http://dx.doi.org/10.3390/cells8080901.

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Inflammasomes are cytosolic multiprotein complexes that regulate inflammatory responses to danger stimuli and infection, and their dysregulation is associated with an increasing number of autoinflammatory diseases. In recent years, zebrafish models of human pathologies to study inflammasome function in vivo have started to emerge. Here, we discuss inflammasome research in zebrafish in light of current knowledge about mammalian inflammasomes. We summarize the evolutionary conservation of inflammasome components between zebrafish and mammals, highlighting the similarities and possible divergence

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10

Yi, Young-Su. "Caspase-11 Non-Canonical Inflammasome: Emerging Activator and Regulator of Infection-Mediated Inflammatory Responses." International Journal of Molecular Sciences 21, no. 8 (2020): 2736. http://dx.doi.org/10.3390/ijms21082736.

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Inflammation is a body’s protective mechanism to eliminate invading pathogens and cellular damaging signals. The inflammatory response consists of two main consecutive steps—a priming step preparing the inflammatory responses and a triggering step boosting the inflammatory responses. The main feature of the triggering step is the activation of the inflammasome, an intracellular multiprotein complex facilitating the inflammatory responses. The regulatory roles of ‘canonical’ inflammasomes in the inflammatory responses and diseases have been largely investigated, so far. New types of inflammasom

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11

Jakob, F., H. J. Girschick, H. Morbach, and C. Hofmann. "Seltene autoinflammatorische Knochenerkrankungen." Arthritis und Rheuma 34, no. 06 (2014): 347–55. http://dx.doi.org/10.1055/s-0037-1619120.

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ZusammenfassungAutoinflammatorische Knochenerkrankungen sind gekennzeichnet durch eine entzündliche zelluläre Infiltration des Knochens, Osteoklastenaktivierung, Osteolyse und gesteigertes Knochenremodelling infolge einer aberranten Aktivierung des angeborenen Immunsystems. Der Knochenabbau infolge chronischer Osteomyelitis zeigt die enge Verknüpfung zwischen Immun- und Skelett system. Die Identifizierung von definierten molekularen Defekten bei verschiedenen Erkrankungen konnte bereits zu einem besseren Verständnis der komplexen Interaktion zwischen Knochen und Immunsystem beitragen. Die spor

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12

Zhang, Zhirong, Gergö Meszaros, Wan-ting He, et al. "Protein kinase D at the Golgi controls NLRP3 inflammasome activation." Journal of Experimental Medicine 214, no. 9 (2017): 2671–93. http://dx.doi.org/10.1084/jem.20162040.

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The inflammasomes are multiprotein complexes sensing tissue damage and infectious agents to initiate innate immune responses. Different inflammasomes containing distinct sensor molecules exist. The NLRP3 inflammasome is unique as it detects a variety of danger signals. It has been reported that NLRP3 is recruited to mitochondria-associated endoplasmic reticulum membranes (MAMs) and is activated by MAM-derived effectors. Here, we show that in response to inflammasome activators, MAMs localize adjacent to Golgi membranes. Diacylglycerol (DAG) at the Golgi rapidly increases, recruiting protein ki

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13

Looi, Chin King, Ling-Wei Hii, Felicia Fei-Lei Chung, Chun-Wai Mai, Wei-Meng Lim, and Chee-Onn Leong. "Roles of Inflammasomes in Epstein–Barr Virus-Associated Nasopharyngeal Cancer." Cancers 13, no. 8 (2021): 1786. http://dx.doi.org/10.3390/cancers13081786.

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Epstein–Barr virus (EBV) infection is recognised as one of the causative agents in most nasopharyngeal carcinoma (NPC) cases. Expression of EBV viral antigens can induce host’s antiviral immune response by activating the inflammasomes to produce pro-inflammatory cytokines, such as interleukin-1β (IL-1β) and IL-18. These cytokines are known to be detrimental to a wide range of virus-infected cells, in which they can activate an inflammatory cell death program, called pyroptosis. However, aberrant inflammasome activation and production of its downstream cytokines lead to chronic inflammation tha

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Ball, Daniel P., Cornelius Y. Taabazuing, Andrew R. Griswold, et al. "Caspase-1 interdomain linker cleavage is required for pyroptosis." Life Science Alliance 3, no. 3 (2020): e202000664. http://dx.doi.org/10.26508/lsa.202000664.

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Pathogen-related signals induce a number of cytosolic pattern-recognition receptors (PRRs) to form canonical inflammasomes, which activate pro-caspase-1 and trigger pyroptotic cell death. All well-studied inflammasome-forming PRRs oligomerize with the adapter protein ASC (apoptosis-associated speck-like protein containing a CARD) to generate a large structure in the cytosol, which induces the dimerization, autoproteolysis, and activation of the pro-caspase-1 zymogen. However, several PRRs can also directly interact with pro-caspase-1 without ASC, forming smaller “ASC-independent” inflammasomes

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15

Nourbakhsh, Fahimeh, Morgayn I. Read, George E. Barreto, and Amirhossein Sahebkar. "Astrocytes and Inflammasome: A Possible Crosstalk in Neurological Diseases." Current Medicinal Chemistry 28, no. 24 (2021): 4972–94. http://dx.doi.org/10.2174/0929867328666210301105422.

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Inflammasome research has primarily focused on neurological tissue, particularly on damaged tissue. Most current neurological literature involves in vivo and in vitro studies utilizing astroglia, as astroglia express the cytoskeletal glial fibrillary acidic protein (GFAP), which is used as a hallmark of neuropathological disorders. Research suggests that astrocytes respond to all forms of neurological damage or disease through reactive astrogliosis. Additionally, there is a consensus among scientists that inflammasomes play an important role in neuroinflammation. This review focuses on the lat

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Di Micco, Antonia, Gianluca Frera, Jérôme Lugrin, et al. "AIM2 inflammasome is activated by pharmacological disruption of nuclear envelope integrity." Proceedings of the National Academy of Sciences 113, no. 32 (2016): E4671—E4680. http://dx.doi.org/10.1073/pnas.1602419113.

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Inflammasomes are critical sensors that convey cellular stress and pathogen presence to the immune system by activating inflammatory caspases and cytokines such as IL-1β. The nature of endogenous stress signals that activate inflammasomes remains unclear. Here we show that an inhibitor of the HIV aspartyl protease, Nelfinavir, triggers inflammasome formation and elicits an IL-1R–dependent inflammation in mice. We found that Nelfinavir impaired the maturation of lamin A, a structural component of the nuclear envelope, thereby promoting the release of DNA in the cytosol. Moreover, deficiency of

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17

Devi, Savita, Christian Stehlik, and Andrea Dorfleutner. "An Update on CARD Only Proteins (COPs) and PYD Only Proteins (POPs) as Inflammasome Regulators." International Journal of Molecular Sciences 21, no. 18 (2020): 6901. http://dx.doi.org/10.3390/ijms21186901.

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Inflammasomes are protein scaffolds required for the activation of caspase-1 and the subsequent release of interleukin (IL)-1β, IL-18, and danger signals, as well as the induction of pyroptotic cell death to restore homeostasis following infection and sterile tissue damage. However, excessive inflammasome activation also causes detrimental inflammatory disease. Therefore, extensive control mechanisms are necessary to prevent improper inflammasome responses and inflammatory disease. Inflammasomes are assembled by sequential nucleated polymerization of Pyrin domain (PYD) and caspase recruitment

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18

El-Sharkawy, Lina Y., David Brough, and Sally Freeman. "Inhibiting the NLRP3 Inflammasome." Molecules 25, no. 23 (2020): 5533. http://dx.doi.org/10.3390/molecules25235533.

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Inflammasomes are protein complexes which are important in several inflammatory diseases. Inflammasomes form part of the innate immune system that triggers the activation of inflammatory cytokines interleukin (IL)-1β and IL-18. The inflammasome most studied in sterile inflammation and non-communicable disease is the NLRP3 inflammasome. Upon activation by diverse pathogen or disease associated signals, NLRP3 nucleates the oligomerization of an adaptor protein ASC forming a platform (the inflammasome) for the recruitment and activation of the protease caspase-1. Active caspase-1 catalyzes the pr

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19

Missiroli, Sonia, Mariasole Perrone, Caterina Boncompagni, et al. "Targeting the NLRP3 Inflammasome as a New Therapeutic Option for Overcoming Cancer." Cancers 13, no. 10 (2021): 2297. http://dx.doi.org/10.3390/cancers13102297.

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Inflammasomes are multiprotein complexes that regulate the maturation and secretion of the proinflammatory cytokines interleukin-1beta (IL-1β and interleukin-18 (IL-18) in response to various intracellular stimuli. As a member of the inflammasomes family, NLRP3 is the most studied and best characterized inflammasome and has been shown to be involved in several pathologies. Recent findings have made it increasingly apparent that the NLRP3 inflammasome may also play a central role in tumorigenesis, and it has attracted attention as a potential anticancer therapy target. In this review, we discus

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Ma, Jialu, Shasha Zhao, Xiao Gao, et al. "The Roles of Inflammasomes in Host Defense against Mycobacterium tuberculosis." Pathogens 10, no. 2 (2021): 120. http://dx.doi.org/10.3390/pathogens10020120.

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Mycobacterium tuberculosis (MTB) infection is characterized by granulomatous lung lesions and systemic inflammatory responses during active disease. Inflammasome activation is involved in regulation of inflammation. Inflammasomes are multiprotein complexes serving a platform for activation of caspase-1, which cleaves the proinflammatory cytokines such as interleukin-1β (IL-1β) and IL-18 into their active forms. These cytokines play an essential role in MTB control. MTB infection triggers activation of the nucleotide-binding domain, leucine-rich-repeat containing family, pyrin domain-containing

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Hayes, Cooper K., Douglas R. Wilcox, Yuchen Yang, Grace K. Coleman, Melissa A. Brown, and Richard Longnecker. "ASC-dependent inflammasomes contribute to immunopathology and mortality in herpes simplex encephalitis." PLOS Pathogens 17, no. 2 (2021): e1009285. http://dx.doi.org/10.1371/journal.ppat.1009285.

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Herpes simplex virus encephalitis (HSE) is the most common cause of sporadic viral encephalitis, and despite targeted antiviral therapy, outcomes remain poor. Although the innate immune system is critical for restricting herpes simplex virus type I (HSV-1) in the brain, there is evidence that prolonged neuroinflammation contributes to HSE pathogenesis. In this study, we investigated the contribution of inflammasomes to disease pathogenesis in a murine model of HSE. Inflammasomes are signaling platforms that activate the pro-inflammatory cytokines interleukin-1β (IL-1β) and IL-18. We found that

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Yang, Qingrui, Chengcheng Yu, Zhaowen Yang, et al. "Deregulated NLRP3 and NLRP1 Inflammasomes and Their Correlations with Disease Activity in Systemic Lupus Erythematosus." Journal of Rheumatology 41, no. 3 (2013): 444–52. http://dx.doi.org/10.3899/jrheum.130310.

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Objective.NOD-like receptor family, pyrin domain containing 3 and 1 (NLRP3 and NLRP1) inflammasomes are molecular platforms that sense the damage or danger signals of cells. We investigated whether NLRP3/NLRP1 inflammasomes are involved in the pathogenesis and progression of systemic lupus erythematosus (SLE).Methods.Expressions of inflammasome components at the mRNA and protein levels in the peripheral blood mononuclear cells (PBMC) from patients with SLE and healthy controls were investigated by quantitative real-time transcription PCR and Western blot, respectively. Correlations between NLR

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23

Hügle, Thomas, and Veit Krenn. "Histo-Pathophysiologie der Gichtarthritis." Therapeutische Umschau 73, no. 3 (2016): 137–40. http://dx.doi.org/10.1024/0040-5930/a000769.

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Zusammenfassung. Gicht ist eine häufige Ursache von entzündlichen Arthritiden und deformierenden Knochenerosionen. Die zugrundeliegende zelluläre und subzelluläre Entzündungsreaktion ist leider nur teilweise verstanden. Das Inflammasom als intrazellulärer Sensor von Uratkristallen führt zur Freisetzung von Interleukin (IL)-1. Histologisch führt die Anreicherung von Uratkristallen in der Synovialmembran zu deren Hyperplasie und zu einer Fibrinablagerung. In einem zweiten Schritt wandern neutrophile Leukozyten ein und es kommt zur Lymphozytenproliferation. Neutrophile Leukozyten induzieren NETs,

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Angosto-Bazarra, Diego, Cristina Molina-López, Alejandro Peñín-Franch, Laura Hurtado-Navarro, and Pablo Pelegrín. "Techniques to Study Inflammasome Activation and Inhibition by Small Molecules." Molecules 26, no. 6 (2021): 1704. http://dx.doi.org/10.3390/molecules26061704.

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Inflammasomes are immune cytosolic oligomers involved in the initiation and progression of multiple pathologies and diseases. The tight regulation of these immune sensors is necessary to control an optimal inflammatory response and recover organism homeostasis. Prolonged activation of inflammasomes result in the development of chronic inflammatory diseases, and the use of small drug-like inhibitory molecules are emerging as promising anti-inflammatory therapies. Different aspects have to be taken in consideration when designing inflammasome inhibitors. This review summarizes the different tech

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Boucher, Dave, Mercedes Monteleone, Rebecca C. Coll, et al. "Caspase-1 self-cleavage is an intrinsic mechanism to terminate inflammasome activity." Journal of Experimental Medicine 215, no. 3 (2018): 827–40. http://dx.doi.org/10.1084/jem.20172222.

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Host-protective caspase-1 activity must be tightly regulated to prevent pathology, but mechanisms controlling the duration of cellular caspase-1 activity are unknown. Caspase-1 is activated on inflammasomes, signaling platforms that facilitate caspase-1 dimerization and autoprocessing. Previous studies with recombinant protein identified a caspase-1 tetramer composed of two p20 and two p10 subunits (p20/p10) as an active species. In this study, we report that in the cell, the dominant species of active caspase-1 dimers elicited by inflammasomes are in fact full-length p46 and a transient speci

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Casson, Cierra N., Janet Yu, Valeria M. Reyes, et al. "Human caspase-4 mediates noncanonical inflammasome activation against gram-negative bacterial pathogens." Proceedings of the National Academy of Sciences 112, no. 21 (2015): 6688–93. http://dx.doi.org/10.1073/pnas.1421699112.

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Inflammasomes are critical for host defense against bacterial pathogens. In murine macrophages infected by gram-negative bacteria, the canonical inflammasome activates caspase-1 to mediate pyroptotic cell death and release of IL-1 family cytokines. Additionally, a noncanonical inflammasome controlled by caspase-11 induces cell death and IL-1 release. However, humans do not encode caspase-11. Instead, humans encode two putative orthologs: caspase-4 and caspase-5. Whether either ortholog functions similar to caspase-11 is poorly defined. Therefore, we sought to define the inflammatory caspases i

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Burton, Eric M., Raphaela Goldbach-Mansky, and Sumita Bhaduri-McIntosh. "A promiscuous inflammasome sparks replication of a common tumor virus." Proceedings of the National Academy of Sciences 117, no. 3 (2020): 1722–30. http://dx.doi.org/10.1073/pnas.1919133117.

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Viruses activate inflammasomes but then subvert resulting inflammatory responses to avoid elimination. We asked whether viruses could instead use such activated or primed inflammasomes to directly aid their propagation and spread. Since herpesviruses are experts at coopting cellular functions, we investigated whether Epstein−Barr virus (EBV), an oncoherpesvirus, exploits inflammasomes to activate its replicative or lytic phase. Indeed, our experiments reveal that EBV exploits several inflammasome sensors to actually activate its replicative phase from quiescence/latency. In particular, TXNIP,

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Finethy, Ryan, Ine Jorgensen, Arun K. Haldar, et al. "Guanylate Binding Proteins Enable Rapid Activation of Canonical and Noncanonical Inflammasomes in Chlamydia-Infected Macrophages." Infection and Immunity 83, no. 12 (2015): 4740–49. http://dx.doi.org/10.1128/iai.00856-15.

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Interferon (IFN)-inducible guanylate binding proteins (GBPs) mediate cell-autonomous host resistance to bacterial pathogens and promote inflammasome activation. The prevailing model postulates that these two GBP-controlled activities are directly linked through GBP-dependent vacuolar lysis. It was proposed that the rupture of pathogen-containing vacuoles (PVs) by GBPs destroyed the microbial refuge and simultaneously contaminated the host cell cytosol with microbial activators of inflammasomes. Here, we demonstrate that GBP-mediated host resistance and GBP-mediated inflammatory responses can b

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Li, Meihe, Tao Sun, Xiaoling Wu, Peng An, Xili Wu, and Huimin Dang. "Autophagy in the HTR-8/SVneo Cell Oxidative Stress Model Is Associated with the NLRP1 Inflammasome." Oxidative Medicine and Cellular Longevity 2021 (March 27, 2021): 1–15. http://dx.doi.org/10.1155/2021/2353504.

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We investigated whether there was activation of NLRP1 inflammasomes and excessive autophagy in oxidative stress damage. And we further demonstrate whether there is a cascade relationship between the activation of NLRP1 inflammasomes and the phenomenon of excessive autophagy. To observe the expression level of the NLRP1 inflammasome group in the pathological process of trophoblast cell oxidative stress, western blot, immunofluorescence, and qRT-PCR were performed. Autophagy in trophoblast cells after the action of H2O2 was detected by using normal trophoblast cells’ NLRP1-specific activator (MD

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Poli, Giulia, Consuelo Fabi, Marina Maria Bellet, et al. "Epigenetic Mechanisms of Inflammasome Regulation." International Journal of Molecular Sciences 21, no. 16 (2020): 5758. http://dx.doi.org/10.3390/ijms21165758.

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The innate immune system represents the host’s first-line defense against pathogens, dead cells or environmental factors. One of the most important inflammatory pathways is represented by the activation of the NOD-like receptor (NLR) protein family. Some NLRs induce the assembly of large caspase-1-activating complexes called inflammasomes. Different types of inflammasomes have been identified that can respond to distinct bacterial, viral or fungal infections; sterile cell damage or other stressors, such as metabolic imbalances. Epigenetic regulation has been recently suggested to provide a com

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Yang, Lijing, Mengjia Hu, Yukai Lu, Songling Han, and Junping Wang. "Inflammasomes and the Maintenance of Hematopoietic Homeostasis: New Perspectives and Opportunities." Molecules 26, no. 2 (2021): 309. http://dx.doi.org/10.3390/molecules26020309.

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Hematopoietic stem cells (HSCs) regularly produce various blood cells throughout life via their self-renewal, proliferation, and differentiation abilities. Most HSCs remain quiescent in the bone marrow (BM) and respond in a timely manner to either physiological or pathological cues, but the underlying mechanisms remain to be further elucidated. In the past few years, accumulating evidence has highlighted an intermediate role of inflammasome activation in hematopoietic maintenance, post-hematopoietic transplantation complications, and senescence. As a cytosolic protein complex, the inflammasome

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Yang, Lijing, Mengjia Hu, Yukai Lu, Songling Han, and Junping Wang. "Inflammasomes and the Maintenance of Hematopoietic Homeostasis: New Perspectives and Opportunities." Molecules 26, no. 2 (2021): 309. http://dx.doi.org/10.3390/molecules26020309.

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Hematopoietic stem cells (HSCs) regularly produce various blood cells throughout life via their self-renewal, proliferation, and differentiation abilities. Most HSCs remain quiescent in the bone marrow (BM) and respond in a timely manner to either physiological or pathological cues, but the underlying mechanisms remain to be further elucidated. In the past few years, accumulating evidence has highlighted an intermediate role of inflammasome activation in hematopoietic maintenance, post-hematopoietic transplantation complications, and senescence. As a cytosolic protein complex, the inflammasome

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Gora, Ilona M., Anna Ciechanowska, and Piotr Ladyzynski. "NLRP3 Inflammasome at the Interface of Inflammation, Endothelial Dysfunction, and Type 2 Diabetes." Cells 10, no. 2 (2021): 314. http://dx.doi.org/10.3390/cells10020314.

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Type 2 diabetes mellitus (T2DM), accounting for 90–95% cases of diabetes, is characterized by chronic inflammation. The mechanisms that control inflammation activation in T2DM are largely unexplored. Inflammasomes represent significant sensors mediating innate immune responses. The aim of this work is to present a review of links between the NLRP3 inflammasome, endothelial dysfunction, and T2DM. The NLRP3 inflammasome activates caspase-1, which leads to the maturation of pro-inflammatory cytokines interleukin 1β and interleukin 18. In this review, we characterize the structure and functions of

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Gram, Anna M., Joost Frenkel, and Maaike E. Ressing. "Inflammasomes and viruses: cellular defence versus viral offence." Journal of General Virology 93, no. 10 (2012): 2063–75. http://dx.doi.org/10.1099/vir.0.042978-0.

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Pro-inflammatory cytokines are important mediators in immune responses against invading pathogens, including viruses. Precursors of the pro-inflammatory cytokines interleukin (IL)-1β and IL-18 are processed by caspase-1. Caspase-1 is activated through autocleavage, but how this is regulated remained elusive for a long time. In 2002, an intracellular multimeric complex was discovered that facilitated caspase-1 cleavage and was termed ‘inflammasome’. To date, different inflammasomes have been described, which recognize a variety of ligands and pathogens. In this review, we discuss the role of in

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Chi, Kun, Xiaodong Geng, Chao Liu, GuangYan Cai, and Quan Hong. "Research Progress on the Role of Inflammasomes in Kidney Disease." Mediators of Inflammation 2020 (January 29, 2020): 1–9. http://dx.doi.org/10.1155/2020/8032797.

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Inflammasomes are multimeric complexes composed of cytoplasmic sensors, apoptosis-associated speck-like protein containing a caspase activation and recruitment domain (ASC or PYCARD), and procaspase-1 and play roles in regulating caspase-dependent inflammation and cell death. Inflammasomes are assembled by sensing pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) and initiate inflammatory responses by activating caspase-1. Activated caspase-1 promotes the release of the inflammatory cytokines interleukin-1β (IL-1β) and IL-18 and eventually induces

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Hoque, Rafaz, and Wajahat Z. Mehal. "Inflammasomes in pancreatic physiology and disease." American Journal of Physiology-Gastrointestinal and Liver Physiology 308, no. 8 (2015): G643—G651. http://dx.doi.org/10.1152/ajpgi.00388.2014.

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In this review we summarize the role of inflammasomes in pancreatic physiology and disease with a focus on acute pancreatitis where much recent progress has been made. New findings have identified inducers of and cell specificity of inflammasome component expression in the pancreas, the contribution of inflammasome-regulated effectors to pancreatitis, and metabolic regulation of inflammasome activation, which are strong determinants of injury in pancreatitis. New areas of pancreatic biology will be highlighted in the context of our evolving understanding of gut microbiome- and injury-induced i

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Feria-Garzón, Manuel G., María T. Rugeles, Juan C. Hernandez, Jorge A. Lujan, and Natalia A. Taborda. "Sulfasalazine as an Immunomodulator of the Inflammatory Process during HIV-1 Infection." International Journal of Molecular Sciences 20, no. 18 (2019): 4476. http://dx.doi.org/10.3390/ijms20184476.

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Background: HIV-1 induces an uncontrolled inflammatory response of several immune components, such as inflammasomes. These molecular complexes, associated with Toll-like receptor (TLR) activity, induce the maturation and release of IL-1β and IL-18 and eventually induce pyroptosis. It has been previously demonstrated that HIV induces inflammasome activation, which is significantly lower in the gastrointestinal tissue and blood from people living with HIV-1 with spontaneous control of viral replication. Therefore, immunomodulatory agents could be useful in improving HIV prognosis. Objective: To

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Magupalli, Venkat Giri, Roberto Negro, Yuzi Tian, et al. "HDAC6 mediates an aggresome-like mechanism for NLRP3 and pyrin inflammasome activation." Science 369, no. 6510 (2020): eaas8995. http://dx.doi.org/10.1126/science.aas8995.

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Inflammasomes are supramolecular complexes that play key roles in immune surveillance. This is accomplished by the activation of inflammatory caspases, which leads to the proteolytic maturation of interleukin 1β (IL-1β) and pyroptosis. Here, we show that nucleotide-binding domain, leucine-rich repeat, and pyrin domain–containing protein 3 (NLRP3)- and pyrin-mediated inflammasome assembly, caspase activation, and IL-1β conversion occur at the microtubule-organizing center (MTOC). Furthermore, the dynein adapter histone deacetylase 6 (HDAC6) is indispensable for the microtubule transport and ass

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Ivanov, Konstantin, Ekaterina Garanina, Albert Rizvanov, and Svetlana Khaiboullina. "Inflammasomes as Targets for Adjuvants." Pathogens 9, no. 4 (2020): 252. http://dx.doi.org/10.3390/pathogens9040252.

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Inflammasomes are an essential part of the innate immune system. They are necessary for the development of a healthy immune response against infectious diseases. Inflammasome activation leads to the secretion of pro-inflammatory cytokines such as IL-1β and IL-18, which stimulate the adaptive immune system. Inflammasomes activators can be used as adjuvants to provide and maintain the strength of the immune response. This review is focused on the mechanisms of action and the effects of adjuvants on inflammasomes. The therapeutic and prophylaxis significance of inflammasomes in infectious disease

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Krakauer, Teresa. "Inflammasomes, Autophagy, and Cell Death: The Trinity of Innate Host Defense against Intracellular Bacteria." Mediators of Inflammation 2019 (January 8, 2019): 1–10. http://dx.doi.org/10.1155/2019/2471215.

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Inflammasome activation is an innate host defense mechanism initiated upon sensing pathogens or danger in the cytosol. Both autophagy and cell death are cell autonomous processes important in development, as well as in host defense against intracellular bacteria. Inflammasome, autophagy, and cell death pathways can be activated by pathogens, pathogen-associated molecular patterns (PAMPs), cell stress, and host-derived damage-associated molecular patterns (DAMPs). Phagocytosis and toll-like receptor (TLR) signaling induce reactive oxygen species (ROS), type I IFN, NFκB activation of proinflamma

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Masood, Humaira, Ruochen Che, and Aihua Zhang. "Inflammasomes in the Pathophysiology of Kidney Diseases." Kidney Diseases 1, no. 3 (2015): 187–93. http://dx.doi.org/10.1159/000438843.

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Background: The inflammasome is a complex of proteins in the cytoplasm that consists of three main components: a sensor protein (receptor), an adapter protein and caspase-1. Inflammasomes are the critical components of innate immunity and have been gradually recognized as a critical mediator in various autoimmune diseases; also, their role in chronic kidney disease and acute kidney injury has been gradually accepted. Summary: Inflammasomes triggered by infectious or sterile injuries transfer proinflammatory mediators into mature ones through innate danger-signaling platforms. Information on in

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Park, Jun Young, Yeo Wool Kang, and Won Gil Cho. "Inflammasome-Mediated Inflammation in Neurodegenerative Diseases." Open Neurology Journal 13, no. 1 (2019): 55–62. http://dx.doi.org/10.2174/1874205x01913010055.

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Inflammasomes are protein platforms consisting of multiple proteins. The biological function includes the activation of caspase-1, leading to the maturation of IL-1β and IL-18. These pro-inflammatory cytokines promote fundamental inflammatory processes in numerous infectious diseases. The inflammasome-mediated inflammation has become increasingly important in central nervous system disorders. In neurodegenerative disorders, significant contributors to disease progression include neuroinflammation and inflammatory cascades initiated by the inflammasome protein complex. This review discusses the

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Tabeeva, G. I., M. R. Dumanovskaya, A. V. Asaturova, I. M. Bogdanova, S. Z. Sanaya, and A. V. Tregubova. "Features of regulation and function of inflammasomes in inflammatory diseases of the female reproductive system." CLINICAL AND EXPERIMENTAL MORPHOLOGY 9, no. 3 (2020): 12–20. http://dx.doi.org/10.31088/cem2020.9.3.12-20.

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Chronic inflammation underlies the progression of many human systemic disorders, including a number of gynecological diseases such as endometriosis and chronic endometritis. Inflammasomes play a special role in the regulation of intercellular interactions under physiological and pathological conditions. The pathogenesis of chronic inflammation assumes a gradual course, accompanied by prolonged maintenance active state of inflammasomes due to the excessive accumulation of intracellular and extracellular endogenous molecules released from destroyed cells – DAMPs (damage-associated molecular patt

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Witola, William H., Ernest Mui, Aubrey Hargrave, et al. "NALP1 Influences Susceptibility to Human Congenital Toxoplasmosis, Proinflammatory Cytokine Response, and Fate ofToxoplasma gondii-Infected Monocytic Cells." Infection and Immunity 79, no. 2 (2010): 756–66. http://dx.doi.org/10.1128/iai.00898-10.

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ABSTRACTNALP1 is a member of the NOD-like receptor (NLR) family of proteins that form inflammasomes. Upon cellular infection or stress, inflammasomes are activated, triggering maturation of proinflammatory cytokines and downstream cellular signaling mediated through the MyD88 adaptor.Toxoplasma gondiiis an obligate intracellular parasite that stimulates production of high levels of proinflammatory cytokines that are important in innate immunity. In this study, susceptibility alleles for human congenital toxoplasmosis were identified in the NALP1 gene. To investigate the role of the NALP1 infla

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Lamkanfi, Mohamed, James L. Mueller, Alberto C. Vitari, et al. "Glyburide inhibits the Cryopyrin/Nalp3 inflammasome." Journal of Cell Biology 187, no. 1 (2009): 61–70. http://dx.doi.org/10.1083/jcb.200903124.

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Inflammasomes activate caspase-1 for processing and secretion of the cytokines interleukin-1β (IL-1β) and IL-18. Cryopyrin/NALP3/NLRP3 is an essential component of inflammasomes triggered by microbial ligands, danger-associated molecular patterns (DAMPs), and crystals. Inappropriate Cryopyrin activity has been incriminated in the pathogenesis of gouty arthritis, Alzheimer's, and silicosis. Therefore, inhibitors of the Nalp3 inflammasome offer considerable therapeutic promise. In this study, we show that the type 2 diabetes drug glyburide prevented activation of the Cryopyrin inflammasome. Glyb

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Hatscher, Lukas, Christian H. K. Lehmann, Ariawan Purbojo, et al. "Select hyperactivating NLRP3 ligands enhance the TH1- and TH17-inducing potential of human type 2 conventional dendritic cells." Science Signaling 14, no. 680 (2021): eabe1757. http://dx.doi.org/10.1126/scisignal.abe1757.

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The detection of microorganisms and danger signals by pattern recognition receptors on dendritic cells (DCs) and the consequent formation of inflammasomes are pivotal for initiating protective immune responses. Although the activation of inflammasomes leading to secretion of the cytokine IL-1β is typically accompanied by pyroptosis (an inflammatory form of lytic programmed cell death), some cells can survive and exist in a state of hyperactivation. Here, we found that the conventional type 2 DC (cDC2) subset is the major human DC subset that is transcriptionally and functionally poised for inf

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Han, Chuanhui, Victoria Godfrey, Zhida Liu, et al. "The AIM2 and NLRP3 inflammasomes trigger IL-1–mediated antitumor effects during radiation." Science Immunology 6, no. 59 (2021): eabc6998. http://dx.doi.org/10.1126/sciimmunol.abc6998.

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The inflammasome promotes inflammation-associated diseases, including cancer, and contributes to the radiation-induced tissue damage. However, the role of inflammasome in radiation-induced antitumor effects is unclear. We observed that tumors transplanted in Casp1−/− mice were resistant to radiation treatment compared with tumors in wild-type (WT) mice. To map out which molecule in the inflammasome pathway contributed to this resistant, we investigated the antitumor effect of radiation in several inflammasome-deficient mice. Tumors grown in either Aim2−/− or Nlrp3−/− mice remained sensitive to

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Li, Yueying, Yuntao Liu, Xia Yan, Qing Liu, Yong-Hua Zhao, and Da-Wei Wang. "Pharmacological Effects and Mechanisms of Chinese Medicines Modulating NLRP3 Inflammasomes in Ischemic Cardio/Cerebral Vascular Disease." American Journal of Chinese Medicine 46, no. 08 (2018): 1727–41. http://dx.doi.org/10.1142/s0192415x18500878.

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Cardio/cerebral-vascular diseases seriously threaten human health and are the leading cause of death. As such, there is great interest in identifying a potential mechanism that controls the development process of cardio/cerebral vascular diseases. Present studies demonstrate that inflammasomes play an important role in the process of ischemic cardio/cerebral vascular diseases (ICCVDs). Among the pathological process of ICCVDs, inflammasomes activated the sterile inflammatory response that accelerated the development of diseases and aggravated the acute lesion of tissue. As the most thoroughly

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Sharma, Deepika, and Thirumala-Devi Kanneganti. "The cell biology of inflammasomes: Mechanisms of inflammasome activation and regulation." Journal of Cell Biology 213, no. 6 (2016): 617–29. http://dx.doi.org/10.1083/jcb.201602089.

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Over the past decade, numerous advances have been made in the role and regulation of inflammasomes during pathogenic and sterile insults. An inflammasome complex comprises a sensor, an adaptor, and a zymogen procaspase-1. The functional output of inflammasome activation includes secretion of cytokines, IL-1β and IL-18, and induction of an inflammatory form of cell death called pyroptosis. Recent studies have highlighted the intersection of this inflammatory response with fundamental cellular processes. Novel modulators and functions of inflammasome activation conventionally associated with the

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Xu, Qiuyun, Xiaorong Zhou, Warren Strober, and Liming Mao. "Inflammasome Regulation: Therapeutic Potential for Inflammatory Bowel Disease." Molecules 26, no. 6 (2021): 1725. http://dx.doi.org/10.3390/molecules26061725.

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Inflammasomes are multiprotein complexes formed to regulate the maturation of pro-inflammatory caspases, in response to intracellular or extracellular stimulants. Accumulating studies showed that the inflammasomes are implicated in the pathogenesis of inflammatory bowel disease (IBD), although their activation is not a decisive factor for the development of IBD. Inflammasomes and related cytokines play an important role in the maintenance of gut immune homeostasis, while its overactivation might induce excess immune responses and consequently cause tissue damage in the gut. Emerging studies pr

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