ArticleCell death discovery2019
Neutrophil extracellular traps induced by VP1 contribute to pulmonary edema during EV71 infection.
Article in Cell death discovery, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Systematic Proteomic Characterization of EV-A71-Infected Mice Identifies Dynamic Molecular Changes and Therapeutic Targets.MedComm · 2026Article
- Distinctive CD39Nature communications · 2024Article
- The key mechanisms of multi-system responses triggered by central nervous system damage in hand, foot, and mouth disease severity.Infectious medicine · 2024Review
- Neutrophil extracellular traps predict postoperative pulmonary complications in paediatric patients undergoing parental liver transplantation.BMC gastroenterology · 2023Article
- Network pharmacology-based exploration identified the antiviral efficacy of Quercetin isolated from mulberry leaves against enterovirus 71 via the NF-κB signaling pathway.Frontiers in pharmacology · 2023Article
- Tight Junctions, the Epithelial Barrier, and Toll-like Receptor-4 During Lung Injury.Inflammation · 2022Review
- Fucosylated oligosaccharide Lacto-Food chemistry: X · 2022Article
- Neutrophils at the crossroads of acute viral infections and severity.Molecular aspects of medicine · 2021Review
- Eosinophil extracellular traps drive asthma progression through neuro-immune signals.Nature cell biology · 2021Article
- The Disruption of the Endothelial Barrier Contributes to Acute Lung Injury Induced byInternational journal of molecular sciences · 2021Article
- Cancer metastasis as a non-healing wound.British journal of cancer · 2021Review
- Neutrophil extracellular traps promote scar formation in post-epidural fibrosis.NPJ Regenerative medicine · 2020Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary edema is a fatal complication of EV71-associated hand, foot, and mouth disease (HFMD). The pathogenesis of EV71-induced pulmonary edema remains largely unclear. In this study, we aimed to explore the roles of the capsid protein VP1 in the occurrence of EV71-induced pulmonary edema. The intranasal inoculation of recombinant VP1 protein caused lung inflammation with an elevation of inflammatory cytokines and neutrophils infiltration. Moreover, neutrophil extracellular traps (NETs) were observed in the lung parenchyma of the mice treated with VP1. VP1 directly induced the formation of NETs, which depended on PAD4. VP1 also damaged the lung barrier via the reduction of the tight junction protein occludin. Moreover, the EV71 attachment receptor vimentin was increased upon VP1 administration. In contrast, NETs decreased vimentin levels, suggesting a novel role for NETs in viral immune defense. These results evidenced a direct role of VP1 in EV71-induced pulmonary edema and demonstrated that NETs may be both harmful and beneficial in EV71 infection.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.