NLRP3 Inflammasome and Inflammatory Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Immunology and Immunotherapy".

Deadline for manuscript submissions: closed (31 March 2024) | Viewed by 2614

Special Issue Editors


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Guest Editor
National Institute of Gastroenterology "S. de Bellis" Research Hospital, Via Turi, 27, 70013 Castellana Grotte, BA, Italy
Interests: inflammation; inflammasome; NLRP3; Gasdermin; gastrointestinal cancers; viral vectors, signaling pathways; genome editing; light and electron microscopy; protein and nucleic acids quantification and analysis; flow-cytometer and cell sorting; cell death assay; immune cell isolation from tissue/biopsy; TRIM-away system; RNAi; cloning; gene overexpression; Elisa; cell biology; intracellular ion fluxes

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Guest Editor
Eberhard Karls University of Tübingen, Medical Faculty, Geschwister-Scholl-Platz, 72074 Tübingen, Germany
Interests: inflammation; innate immunity; pattern-recognition receptors; higher-ordered mac-romolecular assemblies; inflammasomes; NLRP3; inflammation-associated disor-ders; structural biology; cryo-electron microscopy; X-ray crystallography; protein biochemistry; cell biology

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Guest Editor
IRCCS-Istituto Tumori “Giovanni Paolo II”, Viale Orazio Flacco, 65, 70124 Bari, Italy
Interests: oncology; cancer development and progression; inflammation cancer-related; in-flammasome; cell biology; cancer signaling pathways; immunohistochemistry and immunofluorescence; gene expression
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Special Issue Information

Dear Colleagues,

Innate immunity embraces different strategies to overcame potential pathogenic insults. Among them, the NLRP3 inflammasome is emerging as one of the most effective response to sterile and/or microbial dangers in the gastrointestinal tract. NLRP3 pathway involves a cytosolic multi-protein complex, which, upon trigger recognition, it assembles, leading to the activation of caspase-1. Once activated, caspase-1 mediates the maturation of the pro-inflammatory cytokines, pro-IL-1β and IL-18, into their bioactive form (IL-1β and IL-18) as well as the activation of the membrane pore-forming protein gasdermin D, allowing the release of the cytokines into the stream, concomitantly with an inflammatory form of cell death called pyroptosis, thus, providing, in most cases, protection against bacterial and viral infections. However, while NLRP3 inflammasome activation is deleterious in the pathogenesis of inflammatory and metabolic diseases, it has been recently shown that its hyperactivation plays beneficial contributions in numerous gastrointestinal inflammatory-driven diseases, including cancer, as well. It becomes, therefore, crucial a fine tuning of NLRP3 inflammasome activation for maintaining proper cellular homeostasis and health. 

Dr. Roberto Negro
Dr. Liudmila Andreeva
Dr. Concetta Saponaro
Guest Editors

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Keywords

  • inflammasome
  • NLRP3
  • Gasdermins
  • pyroptosis
  • inflammation
  • cancer

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Published Papers (1 paper)

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Research

12 pages, 841 KiB  
Article
Differences and Associations of NLRP3 Inflammasome Levels with Interleukins 1α, 1β, 33 and 37 in Adults with Prediabetes and Type 2 Diabetes Mellitus
by Hend Alfadul, Shaun Sabico, Mohammed G. A. Ansari, Abdullah M. Alnaami, Osama E. Amer, Syed D. Hussain, Kaiser Wani, Malak N. K. Khattak, Mario Clerici and Nasser M. Al-Daghri
Biomedicines 2023, 11(5), 1315; https://doi.org/10.3390/biomedicines11051315 - 28 Apr 2023
Cited by 9 | Viewed by 2123
Abstract
Inflammasome activation of the nucleotide-binding domain, leucine-rich–containing family, and pyrin domain–containing-3 (NLRP3) has been observed to be involved in the pathogenesis of numerous inflammatory diseases, including prediabetes (PD) and type 2 diabetes mellitus (T2DM). Varying levels of glycemia can trigger inflammasome activation; yet, [...] Read more.
Inflammasome activation of the nucleotide-binding domain, leucine-rich–containing family, and pyrin domain–containing-3 (NLRP3) has been observed to be involved in the pathogenesis of numerous inflammatory diseases, including prediabetes (PD) and type 2 diabetes mellitus (T2DM). Varying levels of glycemia can trigger inflammasome activation; yet, limited studies have reported the associations between NLRP3 levels or other circulating interleukins (ILs) and glycemic status. This study investigated the differences and associations between serum levels of NLRP3 and IL-1α, IL-1β, IL-33 and IL-37 in Arab adults with PD and T2DM. A total of 407 Saudi adults (151 males and 256 females) (mean age = 41.4 ± 9.1 years and mean BMI = 30.7 ± 6.4 kg/m2) were included. Overnight-fasting serum samples were collected. The participants were stratified according to T2DM status. Serum levels of NLRP3 and ILs of interest were assessed using commercially available assays. In all participants, age- and BMI-adjusted circulating levels of IL-37 were significantly higher in the T2DM group (p = 0.02) than in healthy controls (HC) and the PD group. A general linear model analysis revealed that NLRP3 levels were significantly influenced by T2DM status; age; and ILs 18, 1α and 33 (p-values 0.03, 0.04, 0.005, 0.004 and 0.007, respectively). IL-1α and triglycerides significantly predicted NLRP3 levels by as much as 46% of the variance perceived (p < 0.01). In conclusion, T2DM status significantly influenced NLRP3 expression and other IL levels in varying degrees. Whether these altered levels of inflammasome markers can be favorably reversed through lifestyle interventions needs to be investigated prospectively in the same population. Full article
(This article belongs to the Special Issue NLRP3 Inflammasome and Inflammatory Diseases)
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