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Biology
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Biology and Function of Inflammasomes
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Biology and Function of Inflammasomes

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Immunology".

Deadline for manuscript submissions: 31 July 2025 | Viewed by 2945

Special Issue Editor

Prof. Dr. Seung-Yong Seong

E-Mail Website
Guest Editor
Department of Biomedical Sciences, Seoul National University College of Medicine, Bio-Medical Science Building 117, 103 Daehak-ro, Jongno-gu, Seoul 03080, Republic of Korea
Interests: inflammasome, innate immunity, inflammation, GPCR19, cancer immunotherapy; single domain antibody therapeutics

Special Issue Information

Dear Colleagues,

Inflammasomes are intracellular multiprotein complexes that play a fundamental role in the immune system. Inflammasomes, comprised of sensors, adaptors, and caspase-1, control the maturation of cytokines (IL-1 and IL-18) and induce pyroptosis. The 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, skin inflammation, and infectious diseases. As inflammasomes respond to a broad range of medically relevant stimuli, inflammasomes have become a highly desirable drug target with which to treat a wide range of human diseases.

This Special Issue, “Biology and Function of Inflammasomes”, welcomes original research and review articles in the field, with a focus on, but not limited to, the molecular basis, pathogenesis, inhibitor development, and therapeutics related to inflammasomes.

Prof. Dr. Seung-Yong Seong
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. Biology 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

  • damage-associated molecular patterns
  • DAMPs
  • pattern recognition receptor
  • immune inflammatory response
  • inflammasome

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Published Papers (3 papers)

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Research

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15 pages, 4814 KiB  
Article
DT-13 Mediates Ligand-Dependent Activation of PPARγ Response Elements In Vitro
by Shikha Raina, Esther Samuel and Hendrik Fuchs
Biology 2024, 13(12), 1015; https://doi.org/10.3390/biology13121015 - 4 Dec 2024
Viewed by 496
Abstract
Activation of inflammatory pathways releases a storm of cytokines. Moreover, unregulated cytokines contribute to chronic inflammatory disorders. However, ligand-activated peroxisome proliferator-activated receptor gamma (PPARγ) is involved in suppressing inflammatory cytokines via transrepression of nuclear factor kappa B (NFκB). Therefore, in this study, the [...] Read more.
Activation of inflammatory pathways releases a storm of cytokines. Moreover, unregulated cytokines contribute to chronic inflammatory disorders. However, ligand-activated peroxisome proliferator-activated receptor gamma (PPARγ) is involved in suppressing inflammatory cytokines via transrepression of nuclear factor kappa B (NFκB). Therefore, in this study, the anti-inflammatory saponin DT-13 is explored as a ligand of PPARγ. DT-13 upregulated the expression of PPARγ in lipopolysaccharide (LPS)-stimulated RAW264.7 cells in comparison to treatment with LPS alone. Applying a HEK transfection model, we observed a DT-13 dose-dependent increase in ligand-dependent activation of PPARγ, which was compared with troglitazone and rosiglitazone. DT-13 was not able to compete with the synthetic fluoromone tracer for binding to PPARγ as observed in a fluorescence polarization binding assay, whereas molecular docking showed a possible binding interaction of DT-13 with the PPARγ nuclear receptor. We proved the expression of PPARγ protein in the presence of DT-13 using a robust cell-based HEK293FT transfection model. More in-depth analysis needs to be performed to evaluate the efficiency of the binding of DT-13 to PPARγ. A possible binding interaction of DT-13 to PPARγ was observed, similar to that of rosiglitazone. This study revealed a novel mechanism for anti-inflammatory effects by DT-13 through PPARγ-dependent transrepression of NFκB. Full article
(This article belongs to the Special Issue Biology and Function of Inflammasomes)
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31 pages, 7275 KiB  
Article
Euterpe oleracea Mart. Bioactive Molecules: Promising Agents to Modulate the NLRP3 Inflammasome
by Carolina Bordin Davidson, Dana El Soufi El Sabbagh, Amanda Kolinski Machado, Lauren Pappis, Michele Rorato Sagrillo, Sabrina Somacal, Tatiana Emanuelli, Júlia Vaz Schultz, João Augusto Pereira da Rocha, André Flores dos Santos, Solange Binotto Fagan, Ivana Zanella da Silva, Ana Cristina Andreazza and Alencar Kolinski Machado
Biology 2024, 13(9), 729; https://doi.org/10.3390/biology13090729 - 17 Sep 2024
Viewed by 1121
Abstract
Inflammation is a vital mechanism that defends the organism against infections and restores homeostasis. However, when inflammation becomes uncontrolled, it leads to chronic inflammation. The NLRP3 inflammasome is crucial in chronic inflammatory responses and has become a focal point in research for new [...] Read more.
Inflammation is a vital mechanism that defends the organism against infections and restores homeostasis. However, when inflammation becomes uncontrolled, it leads to chronic inflammation. The NLRP3 inflammasome is crucial in chronic inflammatory responses and has become a focal point in research for new anti-inflammatory therapies. Flavonoids like catechin, apigenin, and epicatechin are known for their bioactive properties (antioxidant, anti-inflammatory, etc.), but the mechanisms behind their anti-inflammatory actions remain unclear. This study aimed to explore the ability of various flavonoids (isolated and combined) to modulate the NLRP3 inflammasome using in silico and in vitro models. Computer simulations, such as molecular docking, molecular dynamics, and MM/GBSA calculations examined the interactions between bioactive molecules and NLRP3 PYD. THP1 cells were treated with LPS + nigericin to activate NLRP3, followed by flavonoid treatment at different concentrations. THP1-derived macrophages were also treated following NLRP3 activation protocols. The assays included colorimetric, fluorometric, microscopic, and molecular techniques. The results showed that catechin, apigenin, and epicatechin had high binding affinity to NLRP3 PYD, similar to the known NLRP3 inhibitor MCC950. These flavonoids, particularly at 1 µg/mL, 0.1 µg/mL, and 0.01 µg/mL, respectively, significantly reduced LPS + nigericin effects in both cell types and decreased pro-inflammatory cytokine, caspase-1, and NLRP3 gene expression, suggesting their potential as anti-inflammatory agents through NLRP3 modulation. Full article
(This article belongs to the Special Issue Biology and Function of Inflammasomes)
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Review

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20 pages, 3121 KiB  
Review
Understanding the Role of NLRP3 Inflammasome in Acute Pancreatitis
by Konstantinos Papantoniou, Ioanna Aggeletopoulou, Christos Michailides, Ploutarchos Pastras and Christos Triantos
Biology 2024, 13(11), 945; https://doi.org/10.3390/biology13110945 - 18 Nov 2024
Viewed by 637
Abstract
Acute pancreatitis (AP) remains a serious clinical condition, with current treatment options being largely supportive. The discovery of inflammasomes, particularly the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, has significantly advanced our knowledge regarding many inflammatory diseases’ pathogenesis, including AP. The NLRP3 [...] Read more.
Acute pancreatitis (AP) remains a serious clinical condition, with current treatment options being largely supportive. The discovery of inflammasomes, particularly the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, has significantly advanced our knowledge regarding many inflammatory diseases’ pathogenesis, including AP. The NLRP3 inflammasome is central in mediating the inflammatory process in AP through its diverse activation mechanisms and its involvement in multiple signal transduction pathways. This has made NLRP3 an appealing target for novel therapeutic strategies aimed at modulating inflammation in AP. Despite the growing interest in NLRP3 as a therapeutic target, there remains a notable gap in clinical research, with few clinical trials exploring the efficacy of NLRP3 inhibitors in AP. Results of several preclinical studies and animal models are promising and suggest that the use of NLRP3 inhibitors could result in reduced inflammation and improved patient outcomes in AP. Further research is urgently needed to assess their potential benefits, safety, and applicability in human patients and address the underlying inflammatory processes driving AP. Full article
(This article belongs to the Special Issue Biology and Function of Inflammasomes)
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