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Inflammasome 2.0
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Inflammasome 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (15 September 2021) | Viewed by 26303

Special Issue Editor

Prof. Dr. Kuo-Feng Hua

E-Mail Website
Guest Editor
Department of Biotechnology and Animal Science, National Ilan University, Yilan 26047, Taiwan
Interests: inflammation; NLRP3 inflammasome; anti-inflammatory; anti-cancer drug development
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear colleagues,

Inflammasomes are cytosolic caspase-1-containing protein complexes which recognize and respond to pathogen infection and diverse sterile host-derived or environmental danger signals to promote inflammatory disease development. Activation of inflammasomes leads to caspase-1-dependent maturation and release of proinflammatory cytokines IL-1β and IL-18 and promotes Gasdermin D-dependent pyroptotic cell death. Dysregulation of inflammasomes is associated with a number of inflammatory conditions, such as metabolic disorders, diabetes, cardiovascular diseases, neurodegenerative diseases, inflammatory bowel disease, kidney injury, and infectious diseases. As inflammasomes respond to a broad range of medically relevant stimuli, inflammasomes become a highly desirable drug target to treat a wide range of human diseases. Small molecule inhibitors targeting inflammasomes offer a new therapeutic strategy in new drug development. This Special Issue, “Inflammasome”, welcomes original research and review articles in the field, with a focus on but not limited to the molecular and mechanistic basis for inflammasome activation, inflammasome-associated pathogenesis, inflammasome inhibitor development, and inflammasome-specific therapeutics.

Prof. Kuo-Feng Hua
Guest Editor

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Keywords

  • Inflammasome
  • Inflammatory disease
  • Caspase-1
  • Cytokines
  • Pyroptosis
  • NLRP3
  • Inflammasome inhibitor
  • Sterile inflammation

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Published Papers (4 papers)

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Research

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26 pages, 6895 KiB  
Article
NLRP3 Inflammasome Blocking as a Potential Treatment of Central Insulin Resistance in Early-Stage Alzheimer’s Disease
by Yulia K. Komleva, Ilia V. Potapenko, Olga L. Lopatina, Yana V. Gorina, Anatoly Chernykh, Elena D. Khilazheva, Alla B. Salmina and Anton N. Shuvaev
Int. J. Mol. Sci. 2021, 22(21), 11588; https://doi.org/10.3390/ijms222111588 - 27 Oct 2021
Cited by 12 | Viewed by 3527
Abstract
Background: Alzheimer’s disease (AD) is a devastating neurodegenerative disorder. In recent years, attention of researchers has increasingly been focused on studying the role of brain insulin resistance (BIR) in the AD pathogenesis. Neuroinflammation makes a significant contribution to the BIR due to the [...] Read more.
Background: Alzheimer’s disease (AD) is a devastating neurodegenerative disorder. In recent years, attention of researchers has increasingly been focused on studying the role of brain insulin resistance (BIR) in the AD pathogenesis. Neuroinflammation makes a significant contribution to the BIR due to the activation of NLRP3 inflammasome. This study was devoted to the understanding of the potential therapeutic roles of the NLRP3 inflammasome in neurodegeneration occurring concomitant with BIR and its contribution to the progression of emotional disorders. Methods: To test the impact of innate immune signaling on the changes induced by Aβ1-42 injection, we analyzed animals carrying a genetic deletion of the Nlrp3 gene. Thus, we studied the role of NLRP3 inflammasomes in health and neurodegeneration in maintaining brain insulin signaling using behavioral, electrophysiological approaches, immunohistochemistry, ELISA and real-time PCR. Results: We revealed that NLRP3 inflammasomes are required for insulin-dependent glucose transport in the brain and memory consolidation. Conclusions NLRP3 knockout protects mice against the development of BIR: Taken together, our data reveal the protective role of Nlrp3 deletion in the regulation of fear memory and the development of Aβ-induced insulin resistance, providing a novel target for the clinical treatment of this disorder. Full article
(This article belongs to the Special Issue Inflammasome 2.0)
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13 pages, 2908 KiB  
Article
Anakinra Activates Superoxide Dismutase 2 to Mitigate Inflammasome Activity
by Marilena Pariano, Stefania Pieroni, Antonella De Luca, Rossana G. Iannitti, Monica Borghi, Matteo Puccetti, Stefano Giovagnoli, Giorgia Renga, Fiorella D’Onofrio, Marina M. Bellet, Claudia Stincardini, Maria Agnese Della-Fazia, Giuseppe Servillo, Frank L. van de Veerdonk, Claudio Costantini and Luigina Romani
Int. J. Mol. Sci. 2021, 22(12), 6531; https://doi.org/10.3390/ijms22126531 - 18 Jun 2021
Cited by 17 | Viewed by 3483
Abstract
Inflammasomes are powerful cytosolic sensors of environmental stressors and are critical for triggering interleukin-1 (IL-1)-mediated inflammatory responses. However, dysregulation of inflammasome activation may lead to pathological conditions, and the identification of negative regulators for therapeutic purposes is increasingly being recognized. Anakinra, the recombinant [...] Read more.
Inflammasomes are powerful cytosolic sensors of environmental stressors and are critical for triggering interleukin-1 (IL-1)-mediated inflammatory responses. However, dysregulation of inflammasome activation may lead to pathological conditions, and the identification of negative regulators for therapeutic purposes is increasingly being recognized. Anakinra, the recombinant form of the IL-1 receptor antagonist, proved effective by preventing the binding of IL-1 to its receptor, IL-1R1, thus restoring autophagy and dampening NLR family pyrin domain containing 3 (NLRP3) activity. As the generation of mitochondrial reactive oxidative species (ROS) is a critical upstream event in the activation of NLRP3, we investigated whether anakinra would regulate mitochondrial ROS production. By profiling the activation of transcription factors induced in murine alveolar macrophages, we found a mitochondrial antioxidative pathway induced by anakinra involving the manganese-dependent superoxide dismutase (MnSOD) or SOD2. Molecularly, anakinra promotes the binding of SOD2 with the deubiquitinase Ubiquitin Specific Peptidase 36 (USP36) and Constitutive photomorphogenesis 9 (COP9) signalosome, thus increasing SOD2 protein longevity. Functionally, anakinra and SOD2 protects mice from pulmonary oxidative inflammation and infection. On a preclinical level, anakinra upregulates SOD2 in murine models of chronic granulomatous disease (CGD) and cystic fibrosis (CF). These data suggest that protection from mitochondrial oxidative stress may represent an additional mechanism underlying the clinical benefit of anakinra and identifies SOD2 as a potential therapeutic target. Full article
(This article belongs to the Special Issue Inflammasome 2.0)
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Review

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17 pages, 9078 KiB  
Review
Regulation of Caspase-8 Activity at the Crossroads of Pro-Inflammation and Anti-Inflammation
by Jun-Hyuk Han, Jooho Park, Tae-Bong Kang and Kwang-Ho Lee
Int. J. Mol. Sci. 2021, 22(7), 3318; https://doi.org/10.3390/ijms22073318 - 24 Mar 2021
Cited by 34 | Viewed by 8460
Abstract
Caspase-8 has been classified as an apoptotic caspase, and its initial definition was an initiator of extrinsic cell death. During the past decade, the concept of caspase-8 functioning has been changed by findings of its additional roles in diverse biological processes. Although caspase-8 [...] Read more.
Caspase-8 has been classified as an apoptotic caspase, and its initial definition was an initiator of extrinsic cell death. During the past decade, the concept of caspase-8 functioning has been changed by findings of its additional roles in diverse biological processes. Although caspase-8 was not originally thought to be involved in the inflammation process, many recent works have determined that caspase-8 plays an important role in the regulatory functions of inflammatory processes. In this review, we describe the recent advances in knowledge regarding the manner in which caspase-8 modulates the inflammatory responses concerning inflammasome activation, cell death, and cytokine induction. Full article
(This article belongs to the Special Issue Inflammasome 2.0)
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37 pages, 7697 KiB  
Review
Structure, Activation and Regulation of NLRP3 and AIM2 Inflammasomes
by Meenakshi Sharma and Eva de Alba
Int. J. Mol. Sci. 2021, 22(2), 872; https://doi.org/10.3390/ijms22020872 - 16 Jan 2021
Cited by 96 | Viewed by 9783
Abstract
The inflammasome is a three-component (sensor, adaptor, and effector) filamentous signaling platform that shields from multiple pathogenic infections by stimulating the proteolytical maturation of proinflammatory cytokines and pyroptotic cell death. The signaling process initiates with the detection of endogenous and/or external danger signals [...] Read more.
The inflammasome is a three-component (sensor, adaptor, and effector) filamentous signaling platform that shields from multiple pathogenic infections by stimulating the proteolytical maturation of proinflammatory cytokines and pyroptotic cell death. The signaling process initiates with the detection of endogenous and/or external danger signals by specific sensors, followed by the nucleation and polymerization from sensor to downstream adaptor and then to the effector, caspase-1. Aberrant activation of inflammasomes promotes autoinflammatory diseases, cancer, neurodegeneration, and cardiometabolic disorders. Therefore, an equitable level of regulation is required to maintain the equilibrium between inflammasome activation and inhibition. Recent advancement in the structural and mechanistic understanding of inflammasome assembly potentiates the emergence of novel therapeutics against inflammasome-regulated diseases. In this review, we have comprehensively discussed the recent and updated insights into the structure of inflammasome components, their activation, interaction, mechanism of regulation, and finally, the formation of densely packed filamentous inflammasome complex that exists as micron-sized punctum in the cells and mediates the immune responses. Full article
(This article belongs to the Special Issue Inflammasome 2.0)
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