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Cells
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Role of Inflammasome Activation in Innate and Adaptive Immunity
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Role of Inflammasome Activation in Innate and Adaptive Immunity

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: 15 May 2024 | Viewed by 4514

Special Issue Editors

Dr. Juan Pablo de Rivero Vaccari

E-Mail Website
Guest Editor
1. Department of Neurological Surgery and The Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, Miami, FL 33136, USA
2. Neuroscience Graduate Program, University of Miami Miller School of Medicine, Miami, FL 33136, USA
3. Cellular Physiology and Molecular Biophysics Graduate Program, University of Miami Miller School of Medicine, Miami, FL 33136, USA
4. Center for Cognitive Neuroscience and Aging, University of Miami Miller School of Medicine, Miami, FL 33136, USA
Interests: inflammasome; neuroinflammation; traumatic brain injury; spinal cord injury; stroke; Alzheimer’s disease; Parkinson’s disease; biomarkers
Special Issues, Collections and Topics in MDPI journals
Dr. Robert W. Keane

E-Mail Website
Guest Editor
Department of Physiology and Molecular Biophysics, Department of Neurological Surger and The Miami Project to Cure Paralysis, Department of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, FL 33136, USA
Interests: inflammasome; neuroimmunology; traumatic brain injury; spinal cord injury; neuroinflammation
Dr. W. Dalton Dietrich

E-Mail Website
Guest Editor
The Miami Project to Cure Paralysis, 1095 NW 14th Terrace (R-48), Miami, FL 33136, USA
Interests: CNS injury and repair; inflammation; neurodegenerative diseases; clinical translation

Special Issue Information

Dear Colleagues,

A key mediator of early inflammatory events after injury and disease is the inflammasome, a multiprotein complex of the innate immune response, responsible for the activation of caspase-1, processing the cytokines IL-1b and IL-18, and the programmed cell death mechanism of pyroptosis. The inflammasome plays a role in the immune response against infections, autoimmune diseases, neurodegenerative diseases, and trauma. Due to the inflammasome’s involvement in various diseases such as Arthritis, Psoriasis, Colitis, Metabolic Syndrome, Alzheimer’s Disease, Parkinson’s Disease, Multiple Sclerosis or Traumatic Brain Injury, Cerebral Ischemia, among others, the inflammasome has gathered attention from a variety of fields. We invite all scientists working on the inflammasome to participate in this topic. Original research articles, reviews, or shorter perspective articles on all aspects related to the inflammasome are welcome. Articles with insights from a cell and molecular biological perspective are especially welcome. Relevant topics include but are not limited to: inflammasome in autoimmune diseases, inflammasome in infections, inflammasome-mediated/cell death, pyroptosis, inflammasome after injury, biomarkers, metabolic syndrome, cancer, microbiome, animal models, and inflammasomes in neurodegenerative diseases.

Dr. Juan Pablo de Rivero Vaccari
Dr. Robert W. Keane
Dr. W. Dalton Dietrich
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. Cells is an international peer-reviewed open access semimonthly 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

  • inflammasome
  • caspase-1
  • ASC specks
  • pyroptosis
  • innate immunity
  • adaptive immunity
  • sterile inflammation
  • cell death pathways
  • apoptosis
  • autophagy
  • NETosis
  • PANoptosis
  • ferroptosis
  • necroptosis
  • neurodegenerative disease
  • trauma
  • cerebral ischemia
  • biomarkers

Published Papers (3 papers)

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Research

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17 pages, 2992 KiB  
Article
The Role of NLRP3 in Regulation of Antimicrobial Peptides and Estrogen Signaling in UPEC-Infected Bladder Epithelial Cells
by Anna Lindblad, Rongrong Wu, Katarina Persson and Isak Demirel
Cells 2023, 12(18), 2298; https://doi.org/10.3390/cells12182298 - 18 Sep 2023
Cited by 1 | Viewed by 1150
Abstract
The NLRP3 inflammasome, estrogen and antimicrobial peptides have all been found to have a vital role in the protection of the bladder urothelium. However, the interdependence between these protective factors during a bladder infection is currently unknown. Our aim was to investigate the [...] Read more.
The NLRP3 inflammasome, estrogen and antimicrobial peptides have all been found to have a vital role in the protection of the bladder urothelium. However, the interdependence between these protective factors during a bladder infection is currently unknown. Our aim was to investigate the role of NLRP3 in the regulation of antimicrobial peptides and estrogen signaling in bladder epithelial cells during a UPEC infection. Human bladder epithelial cells and CRISPR/Cas9-generated NLRP3-deficient cells were stimulated with the UPEC strain CFT073 and estradiol. The gene and protein expression were evaluated with microarray, qRT-PCR, western blot and ELISA. Microarray results showed that the expression of most antimicrobial peptides was reduced in CFT073-infected NLRP3-deficient cells compared to Cas9 control cells. Conditioned medium from NLRP3-deficient cells also lost the ability to suppress CFT073 growth. Moreover, NLRP3-deficient cells had lower basal release of Beta-defensin-1, Beta-defensin-2 and RNase7. The ability of estradiol to induce an increased expression of antimicrobial peptides was also abrogated in NLRP3-deficient cells. The decreased antimicrobial peptide expression might be linked to the observed reduced expression and activity of estradiol receptor beta in NLRP3-deficient cells. This study suggests that NLRP3 may regulate the release and expression of antimicrobial peptides and affect estrogen signaling in bladder epithelial cells. Full article
(This article belongs to the Special Issue Role of Inflammasome Activation in Innate and Adaptive Immunity)
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17 pages, 5160 KiB  
Article
Necrotic Cell Death and Inflammasome NLRP3 Activity in Mycobacterium bovis-Infected Bovine Macrophages
by Omar Escobar-Chavarría, Alejandro Benitez-Guzman, Itzel Jiménez-Vázquez, Jacobo Carrisoza-Urbina, Lourdes Arriaga-Pizano, Sara Huerta-Yépez, Guillermina Baay-Guzmán and José A. Gutiérrez-Pabello
Cells 2023, 12(16), 2079; https://doi.org/10.3390/cells12162079 - 17 Aug 2023
Viewed by 1280
Abstract
Mycobacterium bovis is a facultative intracellular bacterium that produces cellular necrosis in granulomatous lesions in bovines. Although M. bovis-induced inflammation actively participates in granuloma development, its role in necrotic cell death and in bovine macrophages has not been fully explored. In this [...] Read more.
Mycobacterium bovis is a facultative intracellular bacterium that produces cellular necrosis in granulomatous lesions in bovines. Although M. bovis-induced inflammation actively participates in granuloma development, its role in necrotic cell death and in bovine macrophages has not been fully explored. In this study, we evaluate the effect of M. bovis AN5 and its culture filtrate protein extract (CFPE) on inflammasome activation in bovine macrophages and its consequences on cell death. Our results show that both stimuli induce necrotic cell death starting 4 h after incubation. CFPE treatment and M. bovis infection also induce the maturation of IL-1β (>3000 pg/mL), oligomerization of ASC (apoptosis-associated speck-like protein containing CARD), and activation of caspase-1, following the canonical activation pathway of the NLRP3 inflammasome. Inhibiting the oligomerization of NLRP3 and caspase-1 decreases necrosis among the infected or CFPE-stimulated macrophages. Furthermore, histological lymph node sections of bovines naturally infected with M. bovis contained cleaved gasdermin D, mainly in macrophages and giant cells within the granulomas. Finally, the induction of cell death (apoptosis and pyroptosis) decreased the intracellular bacteria count in the infected bovine macrophages, suggesting that cell death helps to control the intracellular growth of the mycobacteria. Our results indicate that M. bovis induces pyroptosis-like cell death that is partially related to the NLRP3 inflammasome activation and that the cell death process could control bacterial growth. Full article
(This article belongs to the Special Issue Role of Inflammasome Activation in Innate and Adaptive Immunity)
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Review

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24 pages, 1047 KiB  
Review
Harnessing Pyroptosis for Cancer Immunotherapy
by Christopher M. Bourne and Cornelius Y. Taabazuing
Cells 2024, 13(4), 346; https://doi.org/10.3390/cells13040346 - 16 Feb 2024
Viewed by 1624
Abstract
Cancer immunotherapy is a novel pillar of cancer treatment that harnesses the immune system to fight tumors and generally results in robust antitumor immunity. Although immunotherapy has achieved remarkable clinical success for some patients, many patients do not respond, underscoring the need to [...] Read more.
Cancer immunotherapy is a novel pillar of cancer treatment that harnesses the immune system to fight tumors and generally results in robust antitumor immunity. Although immunotherapy has achieved remarkable clinical success for some patients, many patients do not respond, underscoring the need to develop new strategies to promote antitumor immunity. Pyroptosis is an immunostimulatory type of regulated cell death that activates the innate immune system. A hallmark of pyroptosis is the release of intracellular contents such as cytokines, alarmins, and chemokines that can stimulate adaptive immune activation. Recent studies suggest that pyroptosis promotes antitumor immunity. Here, we review the mechanisms by which pyroptosis can be induced and highlight new strategies to induce pyroptosis in cancer cells for antitumor defense. We discuss how pyroptosis modulates the tumor microenvironment to stimulate adaptive immunity and promote antitumor immunity. We also suggest research areas to focus on for continued development of pyroptosis as an anticancer treatment. Pyroptosis-based anticancer therapies offer a promising new avenue for treating immunologically ‘cold’ tumors. Full article
(This article belongs to the Special Issue Role of Inflammasome Activation in Innate and Adaptive Immunity)
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