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Inflammation, Inflammatory Diseases, and Inflammasomes
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Inflammation, Inflammatory Diseases, and Inflammasomes

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

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 9612

Special Issue Editors

Dr. Young-Su Yi

E-Mail Website
Guest Editor
Department of Life Sciences, Kyonggi University, Suwon 16227, Republic of Korea
Interests: inflammation; inflammatory/autoimmune diseases; non-canonical inflammasomes; macrophage; anti-inflammatory therapeutics; signaling transduction; immunology; molecular biology; biochemistry
Special Issues, Collections and Topics in MDPI journals
Dr. Miyong Yun

E-Mail Website
Guest Editor
Faculty of Molecular Biology, Sejong University, Seoul 05006, Republic of Korea
Interests: zerumbone; ETBF; BFT; inflammation; nf-κb
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Although inflammation is a body-protective mechanism from pathogen infection and cellular danger signals, chronic inflammation is a major risk factor for various human diseases. Therefore, much effort has been made on demonstrating the mechanisms of inflammatory responses and developing anti-inflammatory therapeutics; however, many studies have mainly focused on the “priming step”, which is a preparatory step of inflammatory responses. Recent studies have discovered another inflammatory step, the “triggering step”, which is an activation step of inflammatory responses. Studies have demonstrated that the key feature of the triggering step is the activation of inflammasomes, which are intracellular protein complexes comprising pattern recognition receptors and inflammatory molecules. Previous studies have demonstrated the roles of inflammasomes in inflammatory responses and many human diseases, providing strong evidence that inflammasomes are the central molecules inducing inflammation and new potential targets for novel anti-inflammatory drug development. However, inflammasome functions and their dysregulation in inflammatory responses and human diseases still need to be investigated.

This Special Issue welcomes original research, reivews, and perspectives with a focus on, but not limited to, the mechanisms of inflammasome regulation, the role of inflammasomes in inflammatory responses and disease, the identification and validation of novel molecules regulating inflammasome functions, and potential inflammasome-targeted therapeutics.

Dr. Young-Su Yi
Dr. Miyong Yun
Guest Editors

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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.

 

Related Special Issue

Published Papers (5 papers)

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Editorial

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3 pages, 176 KiB  
Editorial
Inflammation, Inflammatory Diseases, and Inflammasomes
by Young-Su Yi
Int. J. Mol. Sci. 2023, 24(11), 9224; https://doi.org/10.3390/ijms24119224 - 25 May 2023
Cited by 1 | Viewed by 898
Abstract
Inflammation represents the innate immune response of the body tissues against invading microbes and cellular danger signals, and, in this way, it is beneficial [...] Full article
(This article belongs to the Special Issue Inflammation, Inflammatory Diseases, and Inflammasomes)

Research

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16 pages, 4113 KiB  
Article
Novel Activity of ODZ10117, a STAT3 Inhibitor, for Regulation of NLRP3 Inflammasome Activation
by Ju-Hui Kang, Se-Bin Lee, Jiu Seok, Dong-Hyuk Kim, Gaeun Ma, Jooho Park, Ae Jin Jeong, Sang-Kyu Ye and Tae-Bong Kang
Int. J. Mol. Sci. 2023, 24(7), 6079; https://doi.org/10.3390/ijms24076079 - 23 Mar 2023
Cited by 3 | Viewed by 2171
Abstract
The NLRP3 inflammasome serves as a host defense mechanism against various pathogens, but there is growing evidence linking its activation in sterile condition to diverse inflammatory diseases. Therefore, the identification of specific inhibitors that target NLRP3 inflammasome activation is meaningful and important for [...] Read more.
The NLRP3 inflammasome serves as a host defense mechanism against various pathogens, but there is growing evidence linking its activation in sterile condition to diverse inflammatory diseases. Therefore, the identification of specific inhibitors that target NLRP3 inflammasome activation is meaningful and important for novel therapies for NLRP3 inflammasome-associated diseases. In this study, we identified a chemical compound, namely ODZ10117 (ODZ), that showed NLRP3 inflammasome-targeting anti-inflammatory effects during the screening of a chemical library for anti-inflammatory activity. Although ODZ was initially discovered as a STAT3 inhibitor, here we found it also has inhibitory activity on NLRP3 inflammasome activation. ODZ inhibited the cleavage of caspase-1 and IL-1β-induced canonical NLRP3 inflammasome triggers, but had no effect on those induced by AIM2 or NLRC4 triggers. Mechanistically, ODZ impairs NLRP3 inflammasome activation through the inhibition of NLRP3–NEK7 interaction that is required for inflammasome formation. Moreover, the results obtained from the in silico docking experiment suggested that ODZ targets NLRP3 protein, which provides evidence for the specificity of ODZ to the NLRP3 inflammasome. Furthermore, ODZ administration significantly reduced MSU-induced IL-1β release and the mortality rate of mice with LPS-induced sepsis. Collectively, these results demonstrate a novel effect of ODZ10117 in regulating NLRP3 inflammasome activation both in vitro and in vivo, making it a promising candidate for the treatment of NLRP3-inflammasome-associated immune disorders and cancer. Full article
(This article belongs to the Special Issue Inflammation, Inflammatory Diseases, and Inflammasomes)
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12 pages, 2313 KiB  
Article
Korean Red Ginseng Saponins Play an Anti-Inflammatory Role by Targeting Caspase-11 Non-Canonical Inflammasome in Macrophages
by Hui-Jin Cho, Eojin Kim and Young-Su Yi
Int. J. Mol. Sci. 2023, 24(2), 1077; https://doi.org/10.3390/ijms24021077 - 5 Jan 2023
Cited by 8 | Viewed by 1591
Abstract
We previously reported that Korean red ginseng (KRG) exerts an anti-inflammatory role through inhibiting caspase-11 non-canonical inflammasome in macrophages; however, the components responsible for the anti-inflammatory role remained unclear. This study explored the anti-inflammatory activity of the KRG saponin fraction (KRGSF) in caspase-11 [...] Read more.
We previously reported that Korean red ginseng (KRG) exerts an anti-inflammatory role through inhibiting caspase-11 non-canonical inflammasome in macrophages; however, the components responsible for the anti-inflammatory role remained unclear. This study explored the anti-inflammatory activity of the KRG saponin fraction (KRGSF) in caspase-11 non-canonical inflammasome-activated macrophages. KRGSF inhibited pyroptosis, pro-inflammatory cytokine secretion, and inflammatory mediator production in caspase-11 non-canonical inflammasome-activated J774A.1 cells. A mechanism study revealed that KRGSF-induced anti-inflammatory action was mediated via suppressing the proteolytic activation of caspase-11 and gasdermin D (GSDMD) in caspase-11 non-canonical inflammasome-activated J774A.1 cells. Moreover, KRGSF increased the survival of lethal septic mice. Taken together, these results reveal KRGSF-mediated anti-inflammatory action with a novel mechanism, by inhibiting caspase-11 non-canonical inflammasome in macrophages. Full article
(This article belongs to the Special Issue Inflammation, Inflammatory Diseases, and Inflammasomes)
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Review

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16 pages, 3735 KiB  
Review
The Role of Post-Translational Modifications in Regulation of NLRP3 Inflammasome Activation
by Jing Xia, Songhong Jiang, Shiqi Dong, Yonghong Liao and Yang Zhou
Int. J. Mol. Sci. 2023, 24(7), 6126; https://doi.org/10.3390/ijms24076126 - 24 Mar 2023
Cited by 8 | Viewed by 3067
Abstract
Pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs) induce NLRP3 inflammasome activation, and subsequent formation of active caspase-1 as well as the maturation of interleukin-1β (IL-1β) and gasdermin D (GSDMD), mediating the occurrence of pyroptosis and inflammation. Aberrant NLRP3 inflammasome activation causes [...] Read more.
Pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs) induce NLRP3 inflammasome activation, and subsequent formation of active caspase-1 as well as the maturation of interleukin-1β (IL-1β) and gasdermin D (GSDMD), mediating the occurrence of pyroptosis and inflammation. Aberrant NLRP3 inflammasome activation causes a variety of diseases. Therefore, the NLRP3 inflammasome pathway is a target for prevention and treatment of relative diseases. Recent studies have suggested that NLRP3 inflammasome activity is closely associated with its post-translational modifications (PTMs). This review focuses on PTMs of the components of the NLRP3 inflammasome and the resultant effects on regulation of its activity to provide references for the exploration of the mechanisms by which the NLRP3 inflammasome is activated and controlled. Full article
(This article belongs to the Special Issue Inflammation, Inflammatory Diseases, and Inflammasomes)
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Other

8 pages, 605 KiB  
Brief Report
Dapsone Lowers Neutrophil to Lymphocyte Ratio and Mortality in COVID-19 Patients Admitted to the ICU
by Badar Kanwar, Asif Khattak and Richard E. Kast
Int. J. Mol. Sci. 2022, 23(24), 15563; https://doi.org/10.3390/ijms232415563 - 8 Dec 2022
Cited by 6 | Viewed by 1300
Abstract
Some physicians use dapsone as part of the standard treatment of severe COVID-19 patients entering the ICU, though some do not. To obtain an indication of whether dapsone is helping or not, we undertook a retrospective chart review of 29 consecutive ICU COVID-19 [...] Read more.
Some physicians use dapsone as part of the standard treatment of severe COVID-19 patients entering the ICU, though some do not. To obtain an indication of whether dapsone is helping or not, we undertook a retrospective chart review of 29 consecutive ICU COVID-19 patients receiving dapsone and 30 not receiving dapsone. As we previously reported, of those given dapsone, 9/29 (30%) died, while of those not given dapsone, 18/30 (60%) died. We looked back on that data set to determine if there might be basic laboratory findings in these patients that might give an indication of a mechanism by which dapsone was acting. We found that the neutrophil-to-lymphocyte ratio decreased in 48% of those given dapsone and in 30% of those not given dapsone. We concluded that dapsone might be lowering that ratio. We then reviewed collected data on neutrophil related inflammation pathways on which dapsone might act as presented here. As this was not a controlled study, many variables prevent drawing any conclusions from this work; a formal, randomized controlled study of dapsone in severe COVID-19 is warranted. Full article
(This article belongs to the Special Issue Inflammation, Inflammatory Diseases, and Inflammasomes)
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