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New Advances in Inflammasomes
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New Advances in Inflammasomes

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 June 2024) | Viewed by 13612

Special Issue Editors

Dr. Mariapaola Marino

E-Mail Website
Guest Editor
1. Dipartimento di Medicina e Chirurgia Traslazionale, Sezione di Patologia Generale, Università Cattolica del Sacro Cuore, 00168 Rome, Italy
2. Fondazione Policlinico Universitario “A. Gemelli” IRCCS, 00168 Rome, Italy
Interests: immunology; autoimmunity; inflammation; biomarkers
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Umberto Basile

E-Mail Website
Guest Editor
Head, Clinical Pathology Unit, Hospital “Santa Maria Goretti” ASL Latina, 04100 Latina, Italy
Interests: autoimmunity; cancer; monoclonal gammopathy; minimal residual disease; biomarkers; other biological fluid; new technologies
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The increased morbidity and mortality due to the coronavirus disease 2019 in subjects with chronic conditions and a compromised immune system result from the host–coronavirus interaction, and inflammasomes have been proposed as important players. The activation of inflammasomes, which are multimeric protein complexes, is a crucial component of the innate immune response and is essential for the elimination of pathogens or damaged cells through the secretion of IL-1β and IL-18 and the induction of pyroptosis. However, the dysregulated activation of inflammasomes is involved in the pathogenesis of different autoimmune–autoinflammatory, neurodegenerative, and metabolic disorders that share the common line of inflammation in their pathogenetic fingerprint. Inhibition of inflammasome activation shows therapeutic effects and a wide range of anti-inflammatory compounds are currently being employed. This Special Issue is devoted to the most recent advances in the biology of inflammasomes and their engagement in human diseases.

Potential topics include, but are not limited to:

  • Inflammation;
  • Autoinflammatory diseases;
  • Cardiovascular diseases;
  • Neurodegenerative disorders;
  • Metabolism;
  • Infections;
  • Mechanisms of action;
  • Molecular targeting therapy.

Dr. Mariapaola Marino
Dr. Umberto Basile
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.

Keywords

  • clinical perspectives
  • pyroptosis
  • nod like receptor protein 3
  • inflammatory diseases
  • cytokines
  • inflammasome
  • biomarkers of inflammasome activation

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Published Papers (6 papers)

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Research

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14 pages, 959 KiB  
Article
Evaluating Single-Nucleotide Polymorphisms in Inflammasome Proteins and Serum Levels of IL-18 and IL-1β in Kidney Interstitial Damage in Anti-Neutrophilic Cytoplasmic Antibody-Associated Vasculitis
by Laura Martinez Valenzuela, Anna Vidal-Alabró, Belén Rubio, Paula Antón-Pàmpols, Francisco Gómez-Preciado, Xavier Fulladosa, Josep Maria Cruzado, Juan Torras, Nuria Lloberas and Juliana Draibe
Int. J. Mol. Sci. 2024, 25(12), 6479; https://doi.org/10.3390/ijms25126479 - 12 Jun 2024
Viewed by 877
Abstract
The inflammasome regulates the innate inflammatory response and is involved in autoimmune diseases. In this study, we explored the levels of IL-18 and IL-1β in serum and urine and the influence of various single-nucleotide polymorphisms (SNPs) on kidney lesions at diagnosis in patients [...] Read more.
The inflammasome regulates the innate inflammatory response and is involved in autoimmune diseases. In this study, we explored the levels of IL-18 and IL-1β in serum and urine and the influence of various single-nucleotide polymorphisms (SNPs) on kidney lesions at diagnosis in patients with ANCA-associated vasculitis (AAV) and their clinical outcomes. Ninety-two patients with renal AAV were recruited, and blood and urine were collected at diagnosis. Serum and urine cytokine levels were measured by ELISA. DNA was extracted and genotyped using TaqMan assays for SNPs in several inflammasome genes. Lower serum IL-18 (p = 0.049) and the IL-18 rs187238 G-carrier genotype (p = 0.042) were associated with severe fibrosis. The IL-18 rs1946518 TT genotype was associated with an increased risk of relapse (p = 0.05), whereas GG was related to better renal outcomes (p = 0.031). The rs187238 GG genotype was identified as a risk factor for mortality within the first year after AAV diagnosis, independent of the requirement for dialysis or lung involvement (p = 0.013). We suggest that decreased cytokine levels could be a surrogate marker of scarring and chronicity of the renal lesions, together with the rs187238 GG genotype. If our results are validated, the rs1946518 TT genotype predicts the risk of relapse and renal outcomes during follow-up. Full article
(This article belongs to the Special Issue New Advances in Inflammasomes)
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16 pages, 2531 KiB  
Article
The Prolonged Activation of the p65 Subunit of the NF-Kappa-B Nuclear Factor Sustains the Persistent Effect of Advanced Glycation End Products on Inflammatory Sensitization in Macrophages
by Sayonara Ivana Santos de Assis, Leonardo Szalo Amendola, Maristela Mitiko Okamoto, Guilherme da Silva Ferreira, Rodrigo Tallada Iborra, Danielle Ribeiro Santos, Monique de Fátima Mello Santana, Kelly Gomes Santana, Maria Lucia Correa-Giannella, Denise Frediani Barbeiro, Francisco Garcia Soriano, Ubiratan Fabres Machado and Marisa Passarelli
Int. J. Mol. Sci. 2024, 25(5), 2713; https://doi.org/10.3390/ijms25052713 - 27 Feb 2024
Cited by 4 | Viewed by 1286
Abstract
Advanced glycation end products (AGEs) prime macrophages for lipopolysaccharide (LPS)-induced inflammation. We investigated the persistence of cellular AGE-sensitization to LPS, considering the nuclear content of p50 and p65 nuclear factor kappa B (NFKB) subunits and the expression of inflammatory genes. Macrophages treated with [...] Read more.
Advanced glycation end products (AGEs) prime macrophages for lipopolysaccharide (LPS)-induced inflammation. We investigated the persistence of cellular AGE-sensitization to LPS, considering the nuclear content of p50 and p65 nuclear factor kappa B (NFKB) subunits and the expression of inflammatory genes. Macrophages treated with control (C) or AGE-albumin were rested for varying intervals in medium alone before being incubated with LPS. Comparisons were made using one-way ANOVA or Student t-test (n = 6). AGE-albumin primed macrophages for increased responsiveness to LPS, resulting in elevated levels of TNF, IL-6, and IL-1beta (1.5%, 9.4%, and 5.6%, respectively), compared to C-albumin. TNF, IL-6, and IL-1 beta secretion persisted for up to 24 h even after the removal of AGE-albumin (area under the curve greater by 1.6, 16, and 5.2 times, respectively). The expressions of Il6 and RelA were higher 8 h after albumin removal, and Il6 and Abca1 were higher 24 h after albumin removal. The nuclear content of p50 remained similar, but p65 showed a sustained increase (2.9 times) for up to 24 h in AGE-albumin-treated cells. The prolonged activation of the p65 subunit of NFKB contributes to the persistent effect of AGEs on macrophage inflammatory priming, which could be targeted for therapies to prevent complications based on the AGE–RAGE–NFKB axis. Full article
(This article belongs to the Special Issue New Advances in Inflammasomes)
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23 pages, 1480 KiB  
Article
Mid-Regional Pro-Adrenomedullin Can Predict Organ Failure and Prognosis in Sepsis?
by Silvia Spoto, Stefania Basili, Roberto Cangemi, Giorgio D’Avanzo, Domenica Marika Lupoi, Giulio Francesco Romiti, Josepmaria Argemi, José Ramón Yuste, Felipe Lucena, Luciana Locorriere, Francesco Masini, Giulia Testorio, Rodolfo Calarco, Marta Fogolari, Maria Francesconi, Giulia Battifoglia, Sebastiano Costantino and Silvia Angeletti
Int. J. Mol. Sci. 2023, 24(24), 17429; https://doi.org/10.3390/ijms242417429 - 13 Dec 2023
Cited by 2 | Viewed by 2059
Abstract
Sepsis causes immune dysregulation and endotheliitis, with an increase in mid-regional pro-adrenomedullin (MR-proADM). The aim of the study is to determine an MR-proADM value that, in addition to clinical diagnosis, can identify patients with localized infection or those with sepsis/septic shock, with specific [...] Read more.
Sepsis causes immune dysregulation and endotheliitis, with an increase in mid-regional pro-adrenomedullin (MR-proADM). The aim of the study is to determine an MR-proADM value that, in addition to clinical diagnosis, can identify patients with localized infection or those with sepsis/septic shock, with specific organ damage or with the need for intensive care unit (ICU) transfer and prognosis. The secondary aim is to correlate the MR-proADM value with the length of stay (LOS). In total, 301 subjects with sepsis (124/301 with septic shock) and 126 with localized infection were retrospectively included. In sepsis, MR-proADM ≥ 3.39 ng/mL identified acute kidney injury (AKI); ≥2.99 ng/mL acute respiratory distress syndrome (ARDS); ≥2.28 ng/mL acute heart failure (AHF); ≥2.55 ng/mL Glascow Coma Scale (GCS) < 15; ≥3.38 multi-organ involvement; ≥3.33 need for ICU transfer; ≥2.0 Sequential Organ Failure Assessment (SOFA) score ≥ 2; and ≥3.15 ng/mL non-survivors. The multivariate analysis showed that MR-proADM ≥ 2 ng/mL correlates with AKI, anemia and SOFA score ≥ 2, and MR-proADM ≥ 3 ng/mL correlates with AKI, GCS < 15 and SOFA score ≥ 2. A correlation between mortality and AKI, GCS < 15, ICU transfer and cathecolamine administration was found. In localized infection, MR-proADM at admission ≥ 1.44 ng/mL identified patients with AKI; ≥1.0 ng/mL with AHF; and ≥1.44 ng/mL with anemia and SOFA score ≥ 2. In the multivariate analysis, MR-proADM ≥ 1.44 ng/mL correlated with AKI, anemia, SOFA score ≥ 2 and AHF. MR-proADM is a marker of oxidative stress due to an infection, reflecting severity proportionally to organ damage. Full article
(This article belongs to the Special Issue New Advances in Inflammasomes)
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Review

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18 pages, 1933 KiB  
Review
The Role of the Immune System in the Course of Hashimoto’s Thyroiditis: The Current State of Knowledge
by Karolina Wrońska, Maciej Hałasa and Małgorzata Szczuko
Int. J. Mol. Sci. 2024, 25(13), 6883; https://doi.org/10.3390/ijms25136883 - 23 Jun 2024
Cited by 3 | Viewed by 4427
Abstract
The process of thyroid autoimmunization develops against the background of genetic predispositions associated with class II human leukocyte antigens (HLA-DR), as well as cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), protein tyrosine phosphatase non-receptor type 22 (PTPN22), and forkhead transcription box protein P3 (FOXP3). Environmental [...] Read more.
The process of thyroid autoimmunization develops against the background of genetic predispositions associated with class II human leukocyte antigens (HLA-DR), as well as cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), protein tyrosine phosphatase non-receptor type 22 (PTPN22), and forkhead transcription box protein P3 (FOXP3). Environmental factors, such as vitamin D deficiency, Zn, Se, and Mg, as well as infections, chronic stress, pregnancy, smoking, alcohol, medications, intestinal dysbiosis, and malnutrition, also play an important role. The first stage of autoimmunization involves the accumulation of macrophages and dendritic cells, as well as plasma cells. In the second stage, the mutual interactions of individual cells in the immune system lead to a decrease in the level of CD8+ in favor of CD4+, which intensifies the synthesis of T lymphocyte derivatives, especially Th1, Th17, Tfh, and Tc, reducing the level of Treg. Consequently, the number of the anti-inflammatory cytokines IL10 and IL2 decreases, and the synthesis of the pro-inflammatory cytokines IL-2, Il-12, Il-17, IL-21, IL-22, IFN-γ, and TNF-α increases. The latter two especially trigger the pyroptosis process involving the inflammasome. Activation of the inflammasome by IL-β and IL-18 produced by macrophages is one of the mechanisms of pyroptosis in the course of Hashimoto’s thyroiditis, involving Gram-negative bacteria and NLRC4. In the next step, the apoptosis of thyroid cells is initiated by the intensification of perforin, granzyme, and proteoglycan synthesis by Tc and NK cells. The current findings raise many possibilities regarding interventions related to the inhibition of pro-inflammatory cytokines and the stimulation of anti-inflammatory cytokines produced by both T and B lymphocytes. Furthermore, since there is currently no effective method for treating thyroid autoimmunity, a summary of the review may provide answers regarding the treatment of not only Hashimoto’s thyroiditis, but also other autoimmune diseases associated with autoimmunity. Full article
(This article belongs to the Special Issue New Advances in Inflammasomes)
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14 pages, 1073 KiB  
Review
The Role of Inflammasomes in Heart Failure
by Panayotis K. Vlachakis, Panagiotis Theofilis, Ioannis Kachrimanidis, Konstantinos Giannakopoulos, Maria Drakopoulou, Anastasios Apostolos, Athanasios Kordalis, Ioannis Leontsinis, Konstantinos Tsioufis and Dimitris Tousoulis
Int. J. Mol. Sci. 2024, 25(10), 5372; https://doi.org/10.3390/ijms25105372 - 14 May 2024
Cited by 2 | Viewed by 1495
Abstract
Heart failure (HF) poses a significant world health challenge due to the increase in the aging population and advancements in cardiac care. In the pathophysiology of HF, the inflammasome has been correlated with the development, progression, and complications of HF disease. Discovering biomarkers [...] Read more.
Heart failure (HF) poses a significant world health challenge due to the increase in the aging population and advancements in cardiac care. In the pathophysiology of HF, the inflammasome has been correlated with the development, progression, and complications of HF disease. Discovering biomarkers linked to inflammasomes enhances understanding of HF diagnosis and prognosis. Directing inflammasome signaling emerges as an innovative therapeutic strategy for managing HF. The present review aims to delve into this inflammatory cascade, understanding its role in the development of HF, its potential role as biomarker, as well as the prospects of modulating inflammasomes as a therapeutic approach for HF. Full article
(This article belongs to the Special Issue New Advances in Inflammasomes)
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21 pages, 6293 KiB  
Review
NLRP3 Inflammasome Involvement in Heart, Liver, and Lung Diseases—A Lesson from Cytokine Storm Syndrome
by Cecilia Napodano, Valeria Carnazzo, Valerio Basile, Krizia Pocino, Annunziata Stefanile, Stefania Gallucci, Patrizia Natali, Umberto Basile and Mariapaola Marino
Int. J. Mol. Sci. 2023, 24(23), 16556; https://doi.org/10.3390/ijms242316556 - 21 Nov 2023
Cited by 10 | Viewed by 2543
Abstract
Inflammation and inflammasomes have been proposed as important regulators of the host–microorganism interaction, playing a key role in morbidity and mortality due to the coronavirus disease 2019 (COVID-19) in subjects with chronic conditions and compromised immune system. The inflammasome consists of a multiprotein [...] Read more.
Inflammation and inflammasomes have been proposed as important regulators of the host–microorganism interaction, playing a key role in morbidity and mortality due to the coronavirus disease 2019 (COVID-19) in subjects with chronic conditions and compromised immune system. The inflammasome consists of a multiprotein complex that finely regulates the activation of caspase-1 and the production and secretion of potent pro-inflammatory cytokines such as IL-1β and IL-18. The pyrin containing NOD (nucleotide-binding oligomerization domain) like receptor (NLRP) is a family of intracellular receptors, sensing patterns associated to pathogens or danger signals and NLRP3 inflammasome is the most deeply analyzed for its involvement in the innate and adaptive immune system as well as its contribution to several autoinflammatory and autoimmune diseases. It is highly expressed in leukocytes and up-regulated in sentinel cells upon inflammatory stimuli. NLRP3 expression has also been reported in B and T lymphocytes, in epithelial cells of oral and genital mucosa, in specific parenchymal cells as cardiomyocytes, and keratinocytes, and chondrocytes. It is well known that a dysregulated activation of the inflammasome is involved in the pathogenesis of different disorders that share the common red line of inflammation in their pathogenetic fingerprint. Here, we review the potential roles of the NLRP3 inflammasome in cardiovascular events, liver damage, pulmonary diseases, and in that wide range of systemic inflammatory syndromes named as a cytokine storm. Full article
(This article belongs to the Special Issue New Advances in Inflammasomes)
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