Imperial College London
Alternate

Dr Onn Min Kon

Faculty of Medicine, National Heart & Lung Institute

Professor of Respiratory Medicine
 
 
 
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Contact

 

+44 (0)20 3312 1751onn.kon CV

 
 
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Location

 

Mint WingSt Mary's Campus

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Summary

 

Publications

Citation

BibTex format

@article{Jackson:2014:10.1164/rccm.201406-1039OC,
author = {Jackson, DJ and Makrinioti, H and Rana, BMJ and Shamji, BWH and Trujillo-Torralbo, M-B and Footitt, J and Del-Rosario, J and Telcian, AG and Nikonova, A and Zhu, J and Aniscenko, J and Gogsadze, L and Bakhsoliani, E and Traub, S and Dhariwal, J and Porter, J and Hunt, D and Hunt, T and Hunt, T and Stanciu, LA and Khaitov, M and Bartlett, NW and Edwards, MR and Kon, OM and Mallia, P and Papadopoulos, NG and Akdis, CA and Westwick, J and Edwards, MJ and Cousins, DJ and Walton, RP and Johnston, SL},
doi = {10.1164/rccm.201406-1039OC},
journal = {American Journal of Respiratory and Critical Care Medicine},
pages = {1373--1382},
title = {IL-33-dependent Type 2 inflammation during rhinovirus-induced asthma exacerbations in vivo},
url = {http://dx.doi.org/10.1164/rccm.201406-1039OC},
volume = {190},
year = {2014}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Rationale: Rhinoviruses are the major cause of asthmaexacerbations; however, its underlying mechanisms are poorlyunderstood. We hypothesized that the epithelial cell–derivedcytokine IL-33 plays a central role in exacerbation pathogenesisthrough augmentation of type 2 inflammation.Objectives: To assess whether rhinovirus induces a type 2inflammatory response in asthma in vivo and to define a role for IL-33in this pathway.Methods: We used a human experimental model of rhinovirusinfection and novel airway sampling techniques to measure IL-4, IL-5,IL-13, and IL-33 levels in the asthmatic and healthy airways duringa rhinovirus infection. Additionally, we cultured human T cells and type2 innate lymphoid cells (ILC2s) with the supernatants of rhinovirusinfectedbronchial epithelial cells (BECs) to assess type 2 cytokineproduction in the presence or absence of IL-33 receptor blockade.Measurements and Main Results: IL-4, IL-5, IL-13, and IL-33 areall induced by rhinovirus in the asthmatic airway in vivo and relate toexacerbation severity. Further, induction of IL-33 correlates withviral load and IL-5 and IL-13 levels. Rhinovirus infection of humanprimary BECs induced IL-33, and culture of human T cells and ILC2swith supernatants of rhinovirus-infected BECs strongly inducedtype 2 cytokines. This induction was entirely dependent on IL-33.Conclusions: IL-33 and type 2 cytokines are induced duringa rhinovirus-induced asthma exacerbation in vivo. Virus-inducedIL-33 and IL-33–responsive T cells and ILC2s are key mechanisticlinks between viral infection and exacerbation of asthma. IL-33inhibition is a novel therapeutic approach for asthma exacerbations
AU  - Jackson,DJ
AU  - Makrinioti,H
AU  - Rana,BMJ
AU  - Shamji,BWH
AU  - Trujillo-Torralbo,M-B
AU  - Footitt,J
AU  - Del-Rosario,J
AU  - Telcian,AG
AU  - Nikonova,A
AU  - Zhu,J
AU  - Aniscenko,J
AU  - Gogsadze,L
AU  - Bakhsoliani,E
AU  - Traub,S
AU  - Dhariwal,J
AU  - Porter,J
AU  - Hunt,D
AU  - Hunt,T
AU  - Hunt,T
AU  - Stanciu,LA
AU  - Khaitov,M
AU  - Bartlett,NW
AU  - Edwards,MR
AU  - Kon,OM
AU  - Mallia,P
AU  - Papadopoulos,NG
AU  - Akdis,CA
AU  - Westwick,J
AU  - Edwards,MJ
AU  - Cousins,DJ
AU  - Walton,RP
AU  - Johnston,SL
DO  - 10.1164/rccm.201406-1039OC
EP  - 1382
PY  - 2014///
SN  - 1535-4970
SP  - 1373
TI  - IL-33-dependent Type 2 inflammation during rhinovirus-induced asthma exacerbations in vivo
T2  - American Journal of Respiratory and Critical Care Medicine
UR  - http://dx.doi.org/10.1164/rccm.201406-1039OC
UR  - https://www.atsjournals.org/doi/full/10.1164/rccm.201406-1039OC
UR  - http://hdl.handle.net/10044/1/26522
VL  - 190
ER  -
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