ArticleJCI insight2018
Enterovirus D68 infection induces IL-17-dependent neutrophilic airway inflammation and hyperresponsiveness.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 36 citations in OpenAlex.
- Neutrophilic asthma: advances in experimental models from pathogenesis to therapeutic translation.Molecular medicine (Cambridge, Mass.) · 2026Review
- Salt-inducible kinase 1 is a key gene in suppressing EVD68-induced asthma by modulating antiviral immunity.Genes & diseases · 2026Article
- Clinical Insights and Severity of Enterovirus D68 Respiratory Infections in Vietnamese Children.Open forum infectious diseases · 2026Article
- Respiratory enterovirus D68: virology, clinical surveillance, host-pathogen interactions, and therapeutic prospects.Frontiers in cellular and infection microbiology · 2026Review
- Respiratory infection with Enterovirus D68 induces severe acute lung inflammation in the pediatric ferret model.iScience · 2025Article
- Enterovirus D68-Associated Respiratory Illness in Children.JAMA network open · 2025Observational
- Insights Into Enterovirus D68 Immunology: Unraveling the Mysteries of Host-Pathogen Interactions.Immunity, inflammation and disease · 2025Review
- Viral Determinants of Childhood Asthma Exacerbation Severity and Treatment Response.The journal of allergy and clinical immunology. In practice · 2025Article
- Characterization of Effect of Enterovirus D68 in 129/Sv Mice Deficient in IFN-α/β and/or IFN-γ Receptors.Comparative medicine · 2024Article
- A self-amplifying RNA vaccine prevents enterovirus D68 infection and disease in preclinical models.Science translational medicine · 2024Article
- Enterovirus-D68 - A Reemerging Non-Polio Enterovirus that Causes Severe Respiratory and Neurological Disease in Children.Frontiers in virology (Lausanne, Switzerland) · 2024Article
- Duration of Enterovirus D68 RNA Shedding in the Upper Respiratory Tract and Transmission among Household Contacts, Colorado, USA.Emerging infectious diseases · 2023Article
- The Picornaviridae Family: Knowledge Gaps, Animal Models, Countermeasures, and Prototype Pathogens.The Journal of infectious diseases · 2023Article
- IL-17a-producing γδT cells and NKG2D signaling mediate bacterial endotoxin-induced neonatal lung injury: implications for bronchopulmonary dysplasia.Frontiers in immunology · 2023Article
- Likelihood of hospitalization for a chronic respiratory condition following pediatric infection with enterovirus and rhinovirus strains.Infectious medicine · 2022Article
- Animal Models of Enterovirus D68 Infection and Disease.Journal of virology · 2022Review
- The pathogenesis and virulence of enterovirus-D68 infection.Virulence · 2021Review
- Deficient inflammasome activation permits an exaggerated asthma phenotype in rhinovirus C-infected immature mice.Mucosal immunology · 2021Article
- Rhinovirus C Infection Induces Type 2 Innate Lymphoid Cell Expansion and Eosinophilic Airway Inflammation.Frontiers in immunology · 2021Article
- Transcriptomic Profiling Reveals a Role for TREM-1 Activation in Enterovirus D68 Infection-Induced Proinflammatory Responses.Frontiers in immunology · 2021Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Enterovirus D68 (EV-D68) shares biologic features with rhinovirus (RV). In 2014, a nationwide outbreak of EV-D68 was associated with severe asthma-like symptoms. We sought to develop a mouse model of EV-D68 infection and determine the mechanisms underlying airway disease. BALB/c mice were inoculated intranasally with EV-D68 (2014 isolate), RV-A1B, or sham, alone or in combination with anti-IL-17A or house dust mite (HDM) treatment. Like RV-A1B, lung EV-D68 viral RNA peaked 12 hours after infection. EV-D68 induced airway inflammation, expression of cytokines (TNF-α, IL-6, IL-12b, IL-17A, CXCL1, CXCL2, CXCL10, and CCL2), and airway hyperresponsiveness, which were suppressed by anti-IL-17A antibody. Neutrophilic inflammation and airway responsiveness were significantly higher after EV-D68 compared with RV-A1B infection. Flow cytometry showed increased lineage-, NKp46-, RORγt+ IL-17+ILC3s and γδ T cells in the lungs of EV-D68-treated mice compared with those in RV-treated mice. EV-D68 infection of HDM-exposed mice induced additive or synergistic increases in BAL neutrophils and eosinophils and expression of IL-17, CCL11, IL-5, and Muc5AC. Finally, patients from the 2014 epidemic period with EV-D68 showed significantly higher nasopharyngeal IL-17 mRNA levels compared with patients with RV-A infection. EV-D68 infection induces IL-17-dependent airway inflammation and hyperresponsiveness, which is greater than that generated by RV-A1B, consistent with the clinical picture of severe asthma-like symptoms.
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What Socratic holds
Registered trials
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 Socratic graph.