ArticleVaccines2023
HuNoV Non-Structural Protein P22 Induces Maturation of IL-1β and IL-18 and N-GSDMD-Dependent Pyroptosis through Activating NLRP3 Inflammasome.
Article in Vaccines, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 8 citations in OpenAlex.
- Synergistic Combination of Hypericin-Mediated Photodynamic Therapy and HIF-1α siRNA Inhibits Triple-Negative Breast Cancer via Inducing PANoptosis in vitro.Cancer management and research · 2026Article
- Exercise Alleviates Atherosclerosis Through the Modulation of the NLRP3 Inflammasome.Current molecular medicine · 2026Review
- A novel role of liquid plasma (LP) induced RONS triggers the endoplasmic reticulum stress response and is associated with GSDME-mediated pyroptosis in anaplastic thyroid cancer.Cell communication and signaling : CCS · 2025Article
- PANoptosis: a potential target of atherosclerotic cardiovascular disease.Apoptosis : an international journal on programmed cell death · 2025Review
- Pyroptosis and chemical classification of pyroptotic agents.Molecular diversity · 2025Review
- Olfactory mucosal mesenchymal stem cells delivered by gelatin sponge scaffolds promote functional recovery of spinal cord injury.Frontiers in bioengineering and biotechnology · 2025Article
- The gasdermin family: emerging therapeutic targets in diseases.Signal transduction and targeted therapy · 2024Review
- The link between neutrophils, NETs, and NLRP3 inflammasomes: The dual effect of CD177 and its therapeutic potential in acute respiratory distress syndrome/acute lung injury.Biomolecules & biomedicine · 2024Article
- Geniposide alleviates post-myocardial infarction-induced pyroptosis by modulating the thioredoxin-interacting protein/NLRP3 signaling pathway.CytoJournal · 2024Article
- Advances in research on the impact and mechanisms of pathogenic microorganism infections on pyroptosis.Frontiers in microbiology · 2024Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Norovirus infection is the leading cause of foodborne gastroenteritis worldwide, causing more than 200,000 deaths each year. As a result of a lack of reproducible and robust in vitro culture systems and suitable animal models for human norovirus (HuNoV) infection, the pathogenesis of HuNoV is still poorly understood. In recent years, human intestinal enteroids (HIEs) have been successfully constructed and demonstrated to be able to support the replication of HuNoV. The NLRP3 inflammasome plays a key role in host innate immune responses by activating caspase1 to facilitate IL-1β and IL-18 secretion and N-GSDMD-driven apoptosis, while NLRP3 inflammasome overactivation plays an important role in the development of various inflammatory diseases. Here, we found that HuNoV activated enteric stem cell-derived human intestinal enteroids (HIEs) NLRP3 inflammasome, which was confirmed by transfection of Caco2 cells with full-length cDNA clones of HuNoV. Further, we found that HuNoV non-structural protein P22 activated the NLRP3 inflammasome and then matured IL-1β and IL-18 and processed the cleavage of gasdermin-D (GSDMD) to N-GSDMD, leading to pyroptosis. Besides, berberine (BBR) could ameliorate the pyroptosis caused by HuNoV and P22 by inhibiting NLRP3 inflammasome activation. Together, these results reveal new insights into the mechanisms of inflammation and cell death caused by HuNoV and provide potential treatments.
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