Inflammasomes in Health and Disease

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (31 May 2023) | Viewed by 8466

Special Issue Editor

Thoracic Medicine, Royal Adelaide Hospital, and Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide, South Australia
Interests: chronic inflammatory diseases; zinc biology; sphingolipids; innate immunity; COPD; pulmonary hypertension; cystic fibrosis

Special Issue Information

Dear Colleagues,

The concept of inflammasomes as multiprotein platforms for sensing danger signals, activating IL-1 family cytokines and orchestrating inflammation has become a hot area of research since its introduction by Jürg Tschopp’s team in 2002. Primarily discovered in cell-free and THP-1 cell culture systems, the inflammasome is now considered key to all biological processes that have an inflammatory component. This includes but is not limited to rheumatic and metabolic disorders and many other chronic inflammatory diseases, infections, cancers, aging, neurodegeneration, as well as organ development, wound healing, blood clotting, pain, and taste sensing. During the COVID-19 pandemic, inflammasome studies have become relevant for targeting the cytokine storm and hypercoagulopathy that are major comorbidities and precipitating factors of mortality. For years since the inflammasome’s discovery, scientists have been searching for small synthetic molecules, plant products, monoclonal antibodies, and other novel biologics for drugs targeting injurious excessive inflammasome activation.

The Special Issue entitled “Inflammasomes in Health and Disease” welcomes the submission of original and review articles covering a broad range of aspects related to the physiologic and pathophysiologic roles of inflammasomes. This may include experimental, clinical, or basic mechanistic studies into the inflammasome pathways as well translational studies searching for novel therapeutic and diagnostic applications.

Dr. Hai Bac Tran
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 submissions that pass pre-check are 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. Biomolecules 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 2700 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

  • inflammasome
  • chronic inflammatory diseases
  • innate immunity
  • IL-1 cytokines
  • inflammatory caspases

Published Papers (2 papers)

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Review

14 pages, 1115 KiB  
Review
Microglia NLRP3 Inflammasome and Neuroimmune Signaling in Substance Use Disorders
by Ming-Lei Guo, Soheil Kazemi Roodsari, Yan Cheng, Rachael Elizabeth Dempsey and Wenhui Hu
Biomolecules 2023, 13(6), 922; https://0-doi-org.brum.beds.ac.uk/10.3390/biom13060922 - 31 May 2023
Cited by 4 | Viewed by 2279
Abstract
During the last decade, substance use disorders (SUDs) have been increasingly recognized as neuroinflammation-related brain diseases. Various types of abused drugs (cocaine, methamphetamine, alcohol, opiate-like drugs, marijuana, etc.) can modulate the activation status of microglia and neuroinflammation levels which are involved in the [...] Read more.
During the last decade, substance use disorders (SUDs) have been increasingly recognized as neuroinflammation-related brain diseases. Various types of abused drugs (cocaine, methamphetamine, alcohol, opiate-like drugs, marijuana, etc.) can modulate the activation status of microglia and neuroinflammation levels which are involved in the pathogenesis of SUDs. Several neuroimmune signaling pathways, including TLR/NF-кB, reactive oxygen species, mitochondria dysfunction, as well as autophagy defection, etc., have been implicated in promoting SUDs. Recently, inflammasome-mediated signaling has been identified as playing critical roles in the microglia activation induced by abused drugs. Among the family of inflammasomes, NOD-, LRR-, and pyrin-domain-containing protein 3 (NLRP3) serves the primary research target due to its abundant expression in microglia. NLRP3 has the capability of integrating multiple external and internal inputs and coordinately determining the intensity of microglia activation under various pathological conditions. Here, we summarize the effects of abused drugs on NLRP3 inflammasomes, as well as others, if any. The research on this topic is still at an infant stage; however, the readily available findings suggest that NLRP3 inflammasome could be a common downstream effector stimulated by various types of abused drugs and play critical roles in determining abused-drug-mediated biological effects through enhancing glia–neuron communications. NLRP3 inflammasome might serve as a novel target for ameliorating the development of SUDs. Full article
(This article belongs to the Special Issue Inflammasomes in Health and Disease)
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26 pages, 1838 KiB  
Review
The Mechanism and Regulation of the NLRP3 Inflammasome during Fibrosis
by Carol M. Artlett
Biomolecules 2022, 12(5), 634; https://0-doi-org.brum.beds.ac.uk/10.3390/biom12050634 - 26 Apr 2022
Cited by 11 | Viewed by 4842
Abstract
Fibrosis is often the end result of chronic inflammation. It is characterized by the excessive deposition of extracellular matrix. This leads to structural alterations in the tissue, causing permanent damage and organ dysfunction. Depending on the organ it effects, fibrosis can be a [...] Read more.
Fibrosis is often the end result of chronic inflammation. It is characterized by the excessive deposition of extracellular matrix. This leads to structural alterations in the tissue, causing permanent damage and organ dysfunction. Depending on the organ it effects, fibrosis can be a serious threat to human life. The molecular mechanism of fibrosis is still not fully understood, but the NLRP3 (NOD-, LRR- and pyrin–domain–containing protein 3) inflammasome appears to play a significant role in the pathogenesis of fibrotic disease. The NLRP3 inflammasome has been the most extensively studied inflammatory pathway to date. It is a crucial component of the innate immune system, and its activation mediates the secretion of interleukin (IL)-1β and IL-18. NLRP3 activation has been strongly linked with fibrosis and drives the differentiation of fibroblasts into myofibroblasts by the chronic upregulation of IL-1β and IL-18 and subsequent autocrine signaling that maintains an activated inflammasome. Both IL-1β and IL-18 are profibrotic, however IL-1β can have antifibrotic capabilities. NLRP3 responds to a plethora of different signals that have a common but unidentified unifying trigger. Even after 20 years of extensive investigation, regulation of the NLRP3 inflammasome is still not completely understood. However, what is known about NLRP3 is that its regulation and activation is complex and not only driven by various activators but controlled by numerous post-translational modifications. More recently, there has been an intensive attempt to discover NLRP3 inhibitors to treat chronic diseases. This review addresses the role of the NLRP3 inflammasome in fibrotic disorders across many different tissues. It discusses the relationships of various NLRP3 activators to fibrosis and covers different therapeutics that have been developed, or are currently in development, that directly target NLRP3 or its downstream products as treatments for fibrotic disorders. Full article
(This article belongs to the Special Issue Inflammasomes in Health and Disease)
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