Enterovirus D68 infection induces IL-17–dependent neutrophilic airway inflammation and hyperresponsiveness
dc.contributor.author | Rajput, C | |
dc.contributor.author | Han, M | |
dc.contributor.author | Bentley, JK | |
dc.contributor.author | Lei, J | |
dc.contributor.author | Ishikawa, T | |
dc.contributor.author | Wu, Q | |
dc.contributor.author | Hinde, JL | |
dc.contributor.author | Callear, AP | |
dc.contributor.author | Stillwell, TL | |
dc.contributor.author | Jackson, WT | |
dc.contributor.author | Martin, ET | |
dc.contributor.author | Hershenson, MB | |
dc.coverage.spatial | United States | |
dc.date.accessioned | 2024-01-18T19:14:15Z | |
dc.date.available | 2024-01-18T19:14:15Z | |
dc.date.issued | 2018-08-23 | |
dc.identifier.issn | 2379-3708 | |
dc.identifier.issn | 2379-3708 | |
dc.identifier.uri | https://www.ncbi.nlm.nih.gov/pubmed/30135310 | |
dc.identifier.uri | https://hdl.handle.net/2027.42/192083 | en |
dc.description.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. | |
dc.format.medium | Electronic-eCollection | |
dc.language | eng | |
dc.publisher | American Society for Clinical Investigation | |
dc.relation.haspart | ARTN e121882 | |
dc.subject | Allergy | |
dc.subject | Asthma | |
dc.subject | Cytokines | |
dc.subject | Infectious disease | |
dc.subject | Pulmonology | |
dc.subject | Allergens | |
dc.subject | Animals | |
dc.subject | Asthma | |
dc.subject | Bronchoalveolar Lavage Fluid | |
dc.subject | Cell Line, Tumor | |
dc.subject | Child | |
dc.subject | Child, Preschool | |
dc.subject | Disease Models, Animal | |
dc.subject | Enterovirus | |
dc.subject | Enterovirus D, Human | |
dc.subject | Enterovirus Infections | |
dc.subject | Female | |
dc.subject | Humans | |
dc.subject | Infant | |
dc.subject | Infant, Newborn | |
dc.subject | Interleukin-17 | |
dc.subject | Lung | |
dc.subject | Male | |
dc.subject | Mice | |
dc.subject | Nasopharynx | |
dc.subject | Neutrophils | |
dc.subject | Pyroglyphidae | |
dc.subject | RNA, Messenger | |
dc.title | Enterovirus D68 infection induces IL-17–dependent neutrophilic airway inflammation and hyperresponsiveness | |
dc.type | Article | |
dc.identifier.pmid | 30135310 | |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/192083/2/121882.1-20180823083956-covered-e0fd13ba177f913fd3156f593ead4cfd.pdf | |
dc.identifier.doi | 10.1172/jci.insight.121882 | |
dc.identifier.doi | https://dx.doi.org/10.7302/22083 | |
dc.identifier.source | JCI Insight | |
dc.description.version | Published version | |
dc.date.updated | 2024-01-18T19:14:05Z | |
dc.identifier.orcid | 0000-0001-8865-7979 | |
dc.identifier.orcid | 0000-0001-9436-5593 | |
dc.identifier.volume | 3 | |
dc.identifier.issue | 16 | |
dc.identifier.startpage | 121882 | |
dc.identifier.name-orcid | Rajput, C | |
dc.identifier.name-orcid | Han, M | |
dc.identifier.name-orcid | Bentley, JK; 0000-0001-8865-7979 | |
dc.identifier.name-orcid | Lei, J | |
dc.identifier.name-orcid | Ishikawa, T | |
dc.identifier.name-orcid | Wu, Q | |
dc.identifier.name-orcid | Hinde, JL | |
dc.identifier.name-orcid | Callear, AP | |
dc.identifier.name-orcid | Stillwell, TL | |
dc.identifier.name-orcid | Jackson, WT | |
dc.identifier.name-orcid | Martin, ET | |
dc.identifier.name-orcid | Hershenson, MB; 0000-0001-9436-5593 | |
dc.working.doi | 10.7302/22083 | en |
dc.owningcollname | Pediatrics and Communicable Diseases, Department of |
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