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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: closed (20 October 2024) | Viewed by 11528

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

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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

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Published Papers (6 papers)

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Research

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17 pages, 4939 KiB  
Article
Inflammasome Proteins Are Reliable Biomarkers of the Inflammatory Response in Aneurysmal Subarachnoid Hemorrhage
by Ruby R. Taylor, Robert W. Keane, Begoña Guardiola, Sofía López-Lage, Lesmes Moratinos, W. Dalton Dietrich, Jon Perez-Barcena and Juan Pablo de Rivero Vaccari
Cells 2024, 13(16), 1370; https://doi.org/10.3390/cells13161370 - 17 Aug 2024
Viewed by 935
Abstract
Aneurysmal subarachnoid hemorrhage (aSAH) is caused by abnormal blood vessel dilation and subsequent rupture, resulting in blood pooling in the subarachnoid space. This neurological insult results in the activation of the inflammasome, a multiprotein complex that processes pro-inflammatory interleukin (IL)-1 cytokines leading to [...] Read more.
Aneurysmal subarachnoid hemorrhage (aSAH) is caused by abnormal blood vessel dilation and subsequent rupture, resulting in blood pooling in the subarachnoid space. This neurological insult results in the activation of the inflammasome, a multiprotein complex that processes pro-inflammatory interleukin (IL)-1 cytokines leading to morbidity and mortality. Moreover, increases in inflammasome proteins are associated with clinical deterioration in many neurological diseases. Limited studies have investigated inflammasome protein expression following aSAH. Reliable markers of the inflammatory response associated with aSAH may allow for earlier detection of patients at risk for complications and aid in the identification of novel pharmacologic targets. Here, we investigated whether inflammasome signaling proteins may serve as potential biomarkers of the inflammatory response in aSAH. Serum and cerebrospinal fluid (CSF) from fifteen aSAH subjects and healthy age-matched controls and hydrocephalus (CSF) no-aneurysm controls were evaluated for levels of inflammasome signaling proteins and downstream pro-inflammatory cytokines. Protein measurements were carried out using Simple Plex and Single-Molecule Array (Simoa) technology. The area under the curve (AUC) was calculated using receiver operating characteristics (ROCs) to obtain information on biomarker reliability, specificity, sensitivity, cut-off points, and likelihood ratio. In addition, a Spearman r correlation matrix was performed to determine the correlation between inflammasome protein levels and clinical outcome measures. aSAH subjects demonstrated elevated caspase-1, apoptosis-associated speck-like protein with a caspase recruiting domain (ASC), IL-18 and IL-1β levels in serum, and CSF when compared to controls. Each of these proteins was found to be a promising biomarker of inflammation in aSAH in the CSF. In addition, ASC, caspase-1, and IL-1β were found to be promising biomarkers of inflammation in aSAH in serum. Furthermore, we found that elevated levels of inflammasome proteins in serum are useful to predict worse functional outcomes following aSAH. Thus, the determination of inflammasome protein levels in CSF and serum in aSAH may be utilized as reliable biomarkers of inflammation in aSAH and used clinically to monitor patient outcomes. Full article
(This article belongs to the Special Issue Role of Inflammasome Activation in Innate and Adaptive Immunity)
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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 1631
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
Cited by 4 | Viewed by 1842
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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27 pages, 2628 KiB  
Review
Beyond Inflammation: Role of Pyroptosis Pathway Activation by Gram-Negative Bacteria and Their Outer Membrane Vesicles (OMVs) in the Interaction with the Host Cell
by Silvia Caterina Resta, Flora Guerra, Adelfia Talà, Cecilia Bucci and Pietro Alifano
Cells 2024, 13(21), 1758; https://doi.org/10.3390/cells13211758 - 23 Oct 2024
Viewed by 901
Abstract
Pyroptosis is a gasdermin-mediated pro-inflammatory programmed cell death that, during microbial infections, aims to restrict the spreading of bacteria. Nevertheless, excessive pyroptosis activation leads to inflammation levels that are detrimental to the host. Pathogen-associated molecular patterns (PAMPs) present in bacteria and outer membrane [...] Read more.
Pyroptosis is a gasdermin-mediated pro-inflammatory programmed cell death that, during microbial infections, aims to restrict the spreading of bacteria. Nevertheless, excessive pyroptosis activation leads to inflammation levels that are detrimental to the host. Pathogen-associated molecular patterns (PAMPs) present in bacteria and outer membrane vesicles (OMVs) can trigger pyroptosis pathways in different cell types with different outcomes. Moreover, some pathogens have evolved virulence factors that directly interfere with pyroptosis pathways, like Yersinia pestis YopM and Shigella flexneri IpaH7.8. Other virulence factors, such as those of Neisseria meningitidis, Neisseria gonorrhoeae, Salmonella enterica, and Helicobacter pylori affect pyroptosis pathways indirectly with important differences between pathogenic and commensal species of the same family. These pathogens deserve special attention because of the increasing antimicrobial resistance of S. flexneri and N. gonorrhoeae, the high prevalence of S. enterica and H. pylori, and the life-threatening diseases caused by N. meningitidis and Y. pestis. While inflammation due to macrophage pyroptosis has been extensively addressed, the effects of activation of pyroptosis pathways on modulation of cell cytoskeleton and cell–cell junctions in epithelia and endothelia and on the bacterial crossing of epithelial and endothelial barriers have only been partly investigated. Another important point is the diverse consequences of pyroptosis pathways on calcium influx, like activation of calcium-dependent enzymes and mitochondria dysregulation. This review will discuss the pyroptotic pathways activated by Gram-negative bacteria and their OMVs, analyzing the differences between pathogens and commensal bacteria. Particular attention will also be paid to the experimental models adopted and the main results obtained in the different models. Finally, strategies adopted by pathogens to modulate these pathways will be discussed with a perspective on the use of pyroptosis inhibitors as adjuvants in the treatment of infections. Full article
(This article belongs to the Special Issue Role of Inflammasome Activation in Innate and Adaptive Immunity)
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21 pages, 2901 KiB  
Review
CARD8: A Novel Inflammasome Sensor with Well-Known Anti-Inflammatory and Anti-Apoptotic Activity
by Tugay Karakaya, Marta Slaufova, Michela Di Filippo, Paulina Hennig, Thomas Kündig and Hans-Dietmar Beer
Cells 2024, 13(12), 1032; https://doi.org/10.3390/cells13121032 - 13 Jun 2024
Viewed by 1506
Abstract
Inflammasomes comprise a group of protein complexes with fundamental roles in the induction of inflammation. Upon sensing stress factors, their assembly induces the activation and release of the pro-inflammatory cytokines interleukin (IL)-1β and -18 and a lytic type of cell death, termed pyroptosis. [...] Read more.
Inflammasomes comprise a group of protein complexes with fundamental roles in the induction of inflammation. Upon sensing stress factors, their assembly induces the activation and release of the pro-inflammatory cytokines interleukin (IL)-1β and -18 and a lytic type of cell death, termed pyroptosis. Recently, CARD8 has joined the group of inflammasome sensors. The carboxy-terminal part of CARD8, consisting of a function-to-find-domain (FIIND) and a caspase activation and recruitment domain (CARD), resembles that of NLR family pyrin domain containing 1 (NLRP1), which is recognized as the main inflammasome sensor in human keratinocytes. The interaction with dipeptidyl peptidases 8 and 9 (DPP8/9) represents an activation checkpoint for both sensors. CARD8 and NLRP1 are activated by viral protease activity targeting their amino-terminal region. However, CARD8 also has some unique features compared to the established inflammasome sensors. Activation of CARD8 occurs independently of the inflammasome adaptor protein apoptosis-associated speck-like protein containing a CARD (ASC), leading mainly to pyroptosis rather than the activation and secretion of pro-inflammatory cytokines. CARD8 was also shown to have anti-inflammatory and anti-apoptotic activity. It interacts with, and inhibits, several proteins involved in inflammation and cell death, such as the inflammasome sensor NLRP3, CARD-containing proteins caspase-1 and -9, nucleotide-binding oligomerization domain containing 2 (NOD2), or nuclear factor kappa B (NF-κB). Single nucleotide polymorphisms (SNPs) of CARD8, some of them occurring at high frequencies, are associated with various inflammatory diseases. The molecular mechanisms underlying the different pro- and anti-inflammatory activities of CARD8 are incompletely understood. Alternative splicing leads to the generation of multiple CARD8 protein isoforms. Although the functional properties of these isoforms are poorly characterized, there is evidence that suggests isoform-specific roles. The characterization of the functions of these isoforms, together with their cell- and disease-specific expression, might be the key to a better understanding of CARD8’s different roles in inflammation and inflammatory diseases. Full article
(This article belongs to the Special Issue Role of Inflammasome Activation in Innate and Adaptive Immunity)
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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
Cited by 4 | Viewed by 3806
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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