Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.1
4.9
Journals
IJMS
Special Issues
Roles of Inflammasomes and Methyltransferases in Inflammation
ijms-logo
Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Roles of Inflammasomes and Methyltransferases in Inflammation

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 (31 July 2022) | Viewed by 11158

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, reviews, 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.

 

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Related Special Issues

Published Papers (5 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Editorial

Jump to: Research, Review

3 pages, 175 KiB  
Editorial
Editorial of Special Issue “Roles of Inflammasomes and Methyltransferases in Inflammation”
by Young-Su Yi and Miyong Yun
Int. J. Mol. Sci. 2022, 23(18), 10283; https://doi.org/10.3390/ijms231810283 - 7 Sep 2022
Cited by 1 | Viewed by 935
Abstract
Inflammation is the first line of defense against pathogens and cellular dangers [...] Full article
(This article belongs to the Special Issue Roles of Inflammasomes and Methyltransferases in Inflammation)

Research

Jump to: Editorial, Review

19 pages, 5719 KiB  
Article
Analysis of miRNA Expression Profiling of RIP2 Knockdown in Chicken HD11 Cells When Infected with Avian Pathogenic E. coli (APEC)
by Hongyan Sun, Yuxuan Cao, Yexin Yang, Huan Li and Lujiang Qu
Int. J. Mol. Sci. 2022, 23(13), 7319; https://doi.org/10.3390/ijms23137319 - 30 Jun 2022
Cited by 3 | Viewed by 1665
Abstract
Colibacillosis is an acute and chronic avian disease caused by avian pathogenic E. coli (APEC). Previous studies have demonstrated that RIP2 plays a significant role in APEC infection. Moreover, increasing evidence indicates that microRNAs (miRNAs) are involved in host–pathogen interactions and the immune [...] Read more.
Colibacillosis is an acute and chronic avian disease caused by avian pathogenic E. coli (APEC). Previous studies have demonstrated that RIP2 plays a significant role in APEC infection. Moreover, increasing evidence indicates that microRNAs (miRNAs) are involved in host–pathogen interactions and the immune response. However, the role of miRNAs in the host against APEC infection remains unclear. Herein, we attempted to reveal new miRNAs potentially involved in the regulation of the immune and inflammatory response against APEC infection, with a particular focus on those possibly correlated with RIP2 expression, via miRNA-seq, RT-qPCR, Western blotting, dual-luciferase reporter assay, and CCK-8. The results showed that a total of 93 and 148 differentially expressed (DE) miRNAs were identified in the knockdown of RIP2 cells following APEC infection (shRIP2+APEC) vs. knockdown of RIP2 cells (shRIP2) and shRIP2 vs. wild-type cells (WT), respectively. Among those identified DE miRNAs, the biological function of gga-miR-455-5p was investigated. It was found that gga-miR-455-5p regulated by RIP2 was involved in the immune and inflammatory response against APEC infection via targeting of IRF2 to modulate the expression of type I interferons. Additionally, RIP2 could directly regulate the production of the type I interferons. Altogether, these findings highlighted the crucial role of miRNAs, especially gga-miR-455-5p, in host defense against APEC infection. Full article
(This article belongs to the Special Issue Roles of Inflammasomes and Methyltransferases in Inflammation)
►▼ Show Figures

Figure 1

19 pages, 5033 KiB  
Article
Transcriptional Regulation of RIP2 Gene by NFIB Is Associated with Cellular Immune and Inflammatory Response to APEC Infection
by Hongyan Sun, Naying Li, Jishuang Tan, Huan Li, Jibin Zhang, Lujiang Qu and Susan J. Lamont
Int. J. Mol. Sci. 2022, 23(7), 3814; https://doi.org/10.3390/ijms23073814 - 30 Mar 2022
Cited by 15 | Viewed by 2365
Abstract
Avian pathogenic E. coli (APEC) can cause localized or systemic infection, resulting in large economic losses per year, and impact health of humans. Previous studies showed that RIP2 (receptor interacting serine/threonine kinase 2) and its signaling pathway played an important role in immune [...] Read more.
Avian pathogenic E. coli (APEC) can cause localized or systemic infection, resulting in large economic losses per year, and impact health of humans. Previous studies showed that RIP2 (receptor interacting serine/threonine kinase 2) and its signaling pathway played an important role in immune response against APEC infection. In this study, chicken HD11 cells were used as an in vitro model to investigate the function of chicken RIP2 and the transcription factor binding to the RIP2 core promoter region via gene overexpression, RNA interference, RT-qPCR, Western blotting, dual luciferase reporter assay, CHIP-PCR, CCK-8, and flow cytometry assay following APEC stimulation. Results showed that APEC stimulation promoted RIP2 expression and cells apoptosis, and inhibited cells viability. Knockdown of RIP2 significantly improved cell viability and suppressed the apoptosis of APEC-stimulated cells. Transcription factor NFIB (Nuclear factor I B) and GATA1 (globin transcription factor 1) binding site was identified in the core promoter region of RIP2 from −2300 bp to −1839 bp. However, only NFIB was confirmed to be bound to the core promoter of RIP2. Overexpression of NFIB exacerbated cell injuries with significant reduction in cell viability and increased cell apoptosis and inflammatory cytokines levels, whereas opposite results were observed in NFIB inhibition treatment group. Moreover, RIP2 was up-regulated by NFIB overexpression, and RIP2 silence mitigated the effect of NFIB overexpression in cell apoptosis, inflammation, and activation of NFκB signaling pathways. This study demonstrated that NFIB overexpression accelerated APEC-induced apoptosis and inflammation via up-regulation of RIP2 mediated downstream pathways in chicken HD11 cells. Full article
(This article belongs to the Special Issue Roles of Inflammasomes and Methyltransferases in Inflammation)
►▼ Show Figures

Figure 1

15 pages, 2540 KiB  
Article
Natterin-Induced Neutrophilia Is Dependent on cGAS/STING Activation via Type I IFN Signaling Pathway
by Carla Lima, Aline Ingrid Andrade-Barros, Jefferson Thiago Gonçalves Bernardo, Eniko Balogh, Valerie F. Quesniaux, Bernhard Ryffel and Monica Lopes-Ferreira
Int. J. Mol. Sci. 2022, 23(7), 3600; https://doi.org/10.3390/ijms23073600 - 25 Mar 2022
Cited by 7 | Viewed by 2649
Abstract
Natterin is a potent pro-inflammatory fish molecule, inducing local and systemic IL-1β/IL-1R1-dependent neutrophilia mediated by non-canonical NLRP6 and NLRC4 inflammasome activation in mice, independent of NLRP3. In this work, we investigated whether Natterin activates mitochondrial damage, resulting in self-DNA leaks into the cytosol, [...] Read more.
Natterin is a potent pro-inflammatory fish molecule, inducing local and systemic IL-1β/IL-1R1-dependent neutrophilia mediated by non-canonical NLRP6 and NLRC4 inflammasome activation in mice, independent of NLRP3. In this work, we investigated whether Natterin activates mitochondrial damage, resulting in self-DNA leaks into the cytosol, and whether the DNA sensor cGAS and STING pathway participate in triggering the innate immune response. Employing a peritonitis mouse model, we found that the deficiency of the tlr2/tlr4, myd88 and trif results in decreased neutrophil influx to peritoneal cavities of mice, indicative that in addition to MyD88, TRIF contributes to neutrophilia triggered by TLR4 engagement by Natterin. Next, we demonstrated that gpcr91 deficiency in mice abolished the neutrophil recruitment after Natterin injection, but mice pre-treated with 2-deoxy-d-glucose that blocks glycolysis presented similar infiltration than WT Natterin-injected mice. In addition, we observed that, compared with the WT Natterin-injected mice, DPI and cyclosporin A treated mice had a lower number of neutrophils in the peritoneal exudate. The levels of dsDNA in the supernatant of the peritoneal exudate and processed IL-33 in the supernatant of the peritoneal exudate or cytoplasmic supernatant of the peritoneal cell lysate of WT Natterin-injected mice were several folds higher than those of the control mice. The recruitment of neutrophils to peritoneal cavity 2 h post-Natterin injection was intensely impaired in ifnar KO mice and partially in il-28r KO mice, but not in ifnγr KO mice. Finally, using cgas KO, sting KO, or irf3 KO mice we found that recruitment of neutrophils to peritoneal cavities was virtually abolished in response to Natterin. These findings reveal cytosolic DNA sensors as critical regulators for Natterin-induced neutrophilia. Full article
(This article belongs to the Special Issue Roles of Inflammasomes and Methyltransferases in Inflammation)
►▼ Show Figures

Figure 1

Review

Jump to: Editorial, Research

14 pages, 1876 KiB  
Review
Regulatory Roles of Caspase-11 Non-Canonical Inflammasome in Inflammatory Liver Diseases
by Young-Su Yi
Int. J. Mol. Sci. 2022, 23(9), 4986; https://doi.org/10.3390/ijms23094986 - 30 Apr 2022
Cited by 17 | Viewed by 2880
Abstract
An inflammatory response consists of two consecutive steps: priming and triggering, to prepare and activate inflammatory responses, respectively. The cardinal feature of the triggering step is the activation of intracellular protein complexes called inflammasomes, which provide a platform for the activation of inflammatory [...] Read more.
An inflammatory response consists of two consecutive steps: priming and triggering, to prepare and activate inflammatory responses, respectively. The cardinal feature of the triggering step is the activation of intracellular protein complexes called inflammasomes, which provide a platform for the activation of inflammatory signaling pathways. Despite many studies demonstrating the regulatory roles of canonical inflammasomes in inflammatory liver diseases, the roles of newly discovered non-canonical inflammasomes in inflammatory liver diseases are still largely unknown. Recent studies have reported the regulatory roles of the caspase-11 non-canonical inflammasome in inflammatory liver diseases, providing strong evidence that the caspase-11 non-canonical inflammasome may play key roles in the pathogenesis of inflammatory liver diseases. This review comprehensively discusses the emerging roles of the caspase-11 non-canonical inflammasome in the pathogenesis of inflammatory liver diseases, focusing on non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), and inflammatory liver injuries and its underlying mechanisms. This review highlights the current knowledge on the regulatory roles of the caspase-11 non-canonical inflammasome in inflammatory liver diseases, providing new insights into the development of potential therapeutics to prevent and treat inflammatory liver diseases by targeting the caspase-11 non-canonical inflammasome. Full article
(This article belongs to the Special Issue Roles of Inflammasomes and Methyltransferases in Inflammation)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-5
Back to TopTop