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Cited by 573

The DOI matches its Crossref record; 37 of the 37 references it cites were found in a registry or an index.

IL-33–Dependent Type 2 Inflammation during Rhinovirus-induced Asthma Exacerbations In Vivo

Open access
Jackson, David J., Makrinioti, Heidi, Rana, Batika M. J., Shamji, Betty W. H., Trujillo-Torralbo, Maria-Belen, Footitt, Joseph, Jerico del-Rosario, Telcian, Aurica G., Nikonova, Alexandra, Zhu, Jie, Aniscenko, Julia, Gogsadze, Leila, Bakhsoliani, Eteri, Traub, Stephanie, Dhariwal, Jaideep, Porter, James, Hunt, Duncan, Hunt, Toby, Hunt, Trevor, Stanciu, Luminita A., Khaitov, Musa, Bartlett, Nathan W., Edwards, Michael R., Kon, Onn Min, Mallia, Patrick, Papadopoulos, Nikolaos G., Akdis, Cezmi A., Westwick, John, Edwards, Matthew J., Cousins, David J., Walton, Ross P., Johnston, Sebastian L.·2014·American Journal of Respiratory and Critical Care Medicine
DOI 10.1164/rccm.201406-1039oc
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Abstract

RATIONALE: Rhinoviruses are the major cause of asthma exacerbations; however, its underlying mechanisms are poorly understood. We hypothesized that the epithelial cell-derived cytokine IL-33 plays a central role in exacerbation pathogenesis through augmentation of type 2 inflammation. OBJECTIVES: To assess whether rhinovirus induces a type 2 inflammatory response in asthma in vivo and to define a role for IL-33 in this pathway. METHODS: We used a human experimental model of rhinovirus infection and novel airway sampling techniques to measure IL-4, IL-5, IL-13, and IL-33 levels in the asthmatic and healthy airways during a rhinovirus infection. Additionally, we cultured human T cells and type 2 innate lymphoid cells (ILC2s) with the supernatants of rhinovirus-infected bronchial epithelial cells (BECs) to assess type 2 cytokine production in the presence or absence of IL-33 receptor blockade. MEASUREMENTS AND MAIN RESULTS: IL-4, IL-5, IL-13, and IL-33 are all induced by rhinovirus in the asthmatic airway in vivo and relate to exacerbation severity. Further, induction of IL-33 correlates with viral load and IL-5 and IL-13 levels. Rhinovirus infection of human primary BECs induced IL-33, and culture of human T cells and ILC2s with supernatants of rhinovirus-infected BECs strongly induced type 2 cytokines. This induction was entirely dependent on IL-33. CONCLUSIONS: IL-33 and type 2 cytokines are induced during a rhinovirus-induced asthma exacerbation in vivo. Virus-induced IL-33 and IL-33-responsive T cells and ILC2s are key mechanistic links between viral infection and exacerbation of asthma. IL-33 inhibition is a novel therapeutic approach for asthma exacerbations.

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Metadata

Authors
Jackson, D. J., Makrinioti, H., Rana, B. M. J., Shamji, B. W. H., Trujillo-Torralbo, M.-B., Footitt, J., del-Rosario, J., Telcian, A. G., Nikonova, A., Zhu, J., Aniscenko, J., Gogsadze, L., Bakhsoliani, E., Traub, S., Dhariwal, J., Porter, J., Hunt, D., Hunt, T., Hunt, T., Stanciu, L. A., Khaitov, M., Bartlett, N. W., Edwards, M. R., Kon, O. M., Mallia, P., Papadopoulos, N. G., Akdis, C. A., Westwick, J., Edwards, M. J., Cousins, D. J., Walton, R. P., & Johnston, S. L.
Venue
American Journal of Respiratory and Critical Care Medicine
Publisher
Oxford University Press (OUP)
Published
2014-12-15
Volume
190
Issue
12
Pages
1373-1382
ISSN
  • 1073-449X (ISSN-L)
  • 1535-4970
DOI
10.1164/rccm.201406-1039oc
OpenAlex
W2150925133
Cited by
573
References
37
FWCI
19.45
Type
journal article
Language
en
Open access
green

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The paper
Jackson, D. J., Makrinioti, H., Rana, B. M. J., Shamji, B. W. H., Trujillo-Torralbo, M.-B., Footitt, J., del-Rosario, J., Telcian, A. G., Nikonova, A., Zhu, J., Aniscenko, J., Gogsadze, L., Bakhsoliani, E., Traub, S., Dhariwal, J., Porter, J., Hunt, D., Hunt, T., Hunt, T., . . . Johnston, S. L. (2014). IL-33–Dependent Type 2 Inflammation during Rhinovirus-induced Asthma Exacerbations In Vivo. American Journal of Respiratory and Critical Care Medicine. https://doi.org/10.1164/rccm.201406-1039oc

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.