Special Issue "Mechanisms of Inflammasome Activation"

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 1 August 2019.

Special Issue Editor

Guest Editor
Dr. James Harris

Rheumatology Research Group, Monash University, Melbourne, Australia
Website | E-Mail
Interests: autophagy; inflammasomes; cytokines; MIF

Special Issue Information

Dear Colleagues,

We are putting together a Special Issue of Cells looking at mechanisms of inflammasome regulation, which we hope will include world-class articles on current developments in our understanding of how different inflammasomes are regulated and their importance in health and disease. We welcome contributions, as review articles or original research papers, on this ever-expanding field of research. In particular, recent advancements in our understanding of the mechanistic processes that underpin the activation of different inflammasomes and their regulation —and dysregulation—by both host and pathogen will be covered.

Dr. James Harris
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • IL-1
  • IL-18
  • NLRP3
  • AIM2
  • NLRC4
  • inflammation

Published Papers (2 papers)

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Research

Open AccessArticle
Circulating Cell-Free mtDNA Contributes to AIM2 Inflammasome-Mediated Chronic Inflammation in Patients with Type 2 Diabetes
Received: 7 February 2019 / Revised: 3 April 2019 / Accepted: 6 April 2019 / Published: 8 April 2019
PDF Full-text (1243 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Mitochondrial dysfunction has been implicated in the pathogenesis of insulin resistance and type 2 diabetes. Damaged mitochondria DNA (mtDNA) may have a role in regulating hyperglycemia during type 2 diabetes. Circulating cell-free mitochondria DNA (ccf-mtDNA) was found in serum and plasma from patients [...] Read more.
Mitochondrial dysfunction has been implicated in the pathogenesis of insulin resistance and type 2 diabetes. Damaged mitochondria DNA (mtDNA) may have a role in regulating hyperglycemia during type 2 diabetes. Circulating cell-free mitochondria DNA (ccf-mtDNA) was found in serum and plasma from patients and has been linked to the prognosis factors in various human diseases. However, the role of ccf-mtDNA in chronic inflammation in type 2 diabetes is unclear. In this study, we hypothesized that the ccf-mtDNA levels are associated with chronic inflammation in patients with type 2 diabetes. The mtDNA levels were elevated in the plasma from patients with type 2 diabetes compared to healthy subjects. The elevated mtDNA levels were associated with interleukin-1β (IL-1β) levels in patients with type 2 diabetes. The mtDNA, from patients with type 2 diabetes, induced absent in melanoma 2 (AIM2) inflammasome-dependent caspase-1 activation and IL-1β and IL-18 secretion in macrophages. Our results suggest that the ccf-mtDNA might contribute to AIM2 inflammasome-mediated chronic inflammation in type 2 diabetes. Full article
(This article belongs to the Special Issue Mechanisms of Inflammasome Activation)
Figures

Figure 1

Open AccessArticle
Human Lung Cell Pyroptosis Following Traumatic Brain Injury
Received: 12 December 2018 / Revised: 9 January 2019 / Accepted: 15 January 2019 / Published: 18 January 2019
PDF Full-text (2259 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Approximately 30% of traumatic brain injured patients suffer from acute lung injury or acute respiratory distress syndrome. Our previous work revealed that extracellular vesicle (EV)-mediated inflammasome signaling plays a crucial role in the pathophysiology of traumatic brain injury (TBI)-induced lung injury. Here, serum-derived [...] Read more.
Approximately 30% of traumatic brain injured patients suffer from acute lung injury or acute respiratory distress syndrome. Our previous work revealed that extracellular vesicle (EV)-mediated inflammasome signaling plays a crucial role in the pathophysiology of traumatic brain injury (TBI)-induced lung injury. Here, serum-derived EVs from severe TBI patients were analyzed for particle size, concentration, origin, and levels of the inflammasome component, an apoptosis-associated speck-like protein containing a caspase-recruiting domain (ASC). Serum ASC levels were analyzed from EV obtained from patients that presented lung injury after TBI and compared them to EV obtained from patients that did not show any signs of lung injury. EVs were co-cultured with lung human microvascular endothelial cells (HMVEC-L) to evaluate inflammasome activation and endothelial cell pyroptosis. TBI patients had a significant increase in the number of serum-derived EVs and levels of ASC. Severe TBI patients with lung injury had a significantly higher level of ASC in serum and serum-derived EVs compared to individuals without lung injury. Only EVs isolated from head trauma patients with gunshot wounds were of neural origin. Delivery of serum-derived EVs to HMVEC-L activated the inflammasome and resulted in endothelial cell pyroptosis. Thus, serum-derived EVs and inflammasome proteins play a critical role in the pathogenesis of TBI-induced lung injury, supporting activation of an EV-mediated neural-respiratory inflammasome axis in TBI-induced lung injury. Full article
(This article belongs to the Special Issue Mechanisms of Inflammasome Activation)
Figures

Graphical abstract

Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Author: Qian Yin 

Tentative Title: The roles of guanylate-binding proteins (GBPs) in activation of both canonical and noncanonical inflammasomes

Author: Anita Pinar

Tentative Title: Inflammasome activation during pathological fibrotic diseases

Author: Tae-Bong Kang 

Tentative Title: The role of signal molecules of necroptosis in inflammasome activation

Abstract: Necroptotic cell death is believed to be associated with inflammation due to the release of cellular contents from damaged plasma membrane. However, growing evidences suggest that many of signal molecules known to regulate necroptotic death can also regulate inflammasome activation in a cell-intrinsic manner. Therefore, in this review, I will discuss about the current knowledge regarding the role of signal molecules of necroptosis in inflammasome activation.

Author: Ju-Young Moon

Tentative Title: The role of inflammasome-dependent and -independent NLRP3 in the kidney disease

Abstract: Many studies have investigated the activation of NLRP3 inflammasome in renal diseases, such as diabetic nephropathy, hypertensive kidney disease and rhabdomyolysis induced kidney injury. The regulation of NLRP3 genetically or pharmacologically, the progression of renal diseases was dampened. The NLRP3 inflammasome activated by various endogenous danger associated molecular patterns (DAMPs) in the kidney disease. Hyperuricemia without uric acid crystals acts as a DAMP activated NLRP3 inflammasome through mitochondrial ROS in the renal macrophages and secreted IL-1β affected to increase NF-κB expression in renal tubular cells. Recently, several evidences have shown NLRP3 could have a role in inflammasome-independent way in non-immune cells. Renal tubular cells have considerable amount of the NLRP3 protein but do not contain pro-IL-1β and secrete IL-1β. This review will outline the role of NLRP3 in the kidney disease and evaluate the NLRP3 as the potential therapeutic target.

Author: James Vince, Maryam Rashidi 

Tentative Title: Mechanisms of particle-induced inflammasome activation and cell death

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