ArticleThe Journal of allergy and clinical immunology2022
Spontaneous NLRP3 inflammasome-driven IL-1-β secretion is induced in severe COVID-19 patients and responds to anakinra treatment.
Article in The Journal of allergy and clinical immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 50 citations in OpenAlex.
- ZDHHC18-Mediated Palmitoylation of ORF3a Promotes SARS-CoV-2 Pathogenesis by Antagonizing TRIM16-Mediated Ubiquitination and Proteasomal Degradation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A feedback loop between DNA damage, genomic instability, and cytoplasmic DNA sensing contributes to cytokine production in COVID-19.Archives of virology · 2025Review
- SARS-CoV-2 encoded ORF3a interacts with YY1 to promote latent HCMV reactivation.PLoS pathogens · 2025Article
- Autosomal Dominant Polycystic Kidney Disease-Related Multifocal Renal Cell Carcinoma: A Narrative Iconographic Review.International journal of molecular sciences · 2025Review
- Pharmacological mechanisms of probenecid for SARS-CoV-2 and RSV co-infection: findings of system pharmacology, molecular docking, molecular dynamics simulation, and structure-activity relationship.Frontiers in microbiology · 2025Article
- Hidden players of COVID-19: the evolving roles of SARS-CoV-2 accessory proteins.Frontiers in immunology · 2025Review
- NRICM101 in combatting COVID-19 induced brain fog: Neuroprotective effects and neurovascular integrity preservation in hACE2 mice.Journal of traditional and complementary medicine · 2025Article
- Identification of a histone deacetylase inhibitor as a therapeutic candidate for congenital central hypoventilation syndrome.Molecular therapy. Nucleic acids · 2024Article
- Inborn Error of WAS Presenting with SARS-CoV-2-Related Multisystem Inflammatory Syndrome in Children.Journal of clinical immunology · 2024Article
- Article
- NFκB and NLRP3/NLRC4 inflammasomes regulate differentiation, activation and functional properties of monocytes in response to distinct SARS-CoV-2 proteins.Nature communications · 2024Article
- The Distinct Regulation of the Vitamin D and Aryl Hydrocarbon Receptors in COVID-19.Nutrients · 2024Observational
- SARS-CoV-2 S protein activates NLRP3 inflammasome and deregulates coagulation factors in endothelial and immune cells.Cell communication and signaling : CCS · 2024Article
- SARS-CoV-2 ORF3a Protein as a Therapeutic Target against COVID-19 and Long-Term Post-Infection Effects.Pathogens (Basel, Switzerland) · 2024Review
- Autism spectrum disorder and a possible role of anti-inflammatory treatments: experience in the pediatric allergy/immunology clinic.Frontiers in psychiatry · 2024Review
- An exploratory analysis of associations of genetic variation with the efficacy of tocilizumab in severe COVID-19 patients. A pharmacogenetic study based on next-generation sequencing.Frontiers in pharmacology · 2024Article
- Vitamin D regulates COVID-19 associated severity by suppressing the NLRP3 inflammasome pathway.PloS one · 2024Article
- Caspase-1 activation, IL-1/IL-6 signature and IFNγ-induced chemokines in lungs of COVID-19 patients.Frontiers in immunology · 2024Article
- Altered Ex Vivo NLRP3 Inflammasome Activation Is Associated with 28-Day Mortality in Septic Patients.Viruses · 2023Article
- Immune inhibitory receptor-mediated immune response, metabolic adaptation, and clinical characterization in patients with COVID-19.Scientific reports · 2023Article
Corrections and comments
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Authors and funding
24 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection may result in a severe pneumonia associated with elevation of blood inflammatory parameters, reminiscent of cytokine storm syndrome. Steroidal anti-inflammatory therapies have shown efficacy in reducing mortality in critically ill patients; however, the mechanisms by which SARS-CoV-2 triggers such an extensive inflammation remain unexplained.
objectivesTo dissect the mechanisms underlying SARS-CoV-2-associated inflammation in patients with severe coronavirus disease 2019 (COVID-19), we studied the role of IL-1β, a pivotal cytokine driving inflammatory phenotypes, whose maturation and secretion are regulated by inflammasomes.
methodsWe analyzed nod-like receptor protein 3 pathway activation by means of confocal microscopy, plasma cytokine measurement, cytokine secretion following in vitro stimulation of blood circulating monocytes, and whole-blood RNA sequencing. The role of open reading frame 3a SARS-CoV-2 protein was assessed by confocal microscopy analysis following nucleofection of a monocytic cell line.
resultsWe found that circulating monocytes from patients with COVID-19 display ASC (adaptor molecule apoptotic speck like protein-containing a CARD) specks that colocalize with nod-like receptor protein 3 inflammasome and spontaneously secrete IL-1β in vitro. This spontaneous activation reverts following patient's treatment with the IL-1 receptor antagonist anakinra. Transfection of a monocytic cell line with cDNA coding for the ORF3a SARS-CoV-2 protein resulted in ASC speck formation.
conclusionsThese results provide further evidence that IL-1β targeting could represent an effective strategy in this disease and suggest a mechanistic explanation for the strong inflammatory manifestations associated with COVID-19.
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