Imperial College London
Portrait Picture

DR COEN WIEGMAN

Faculty of Medicine, National Heart & Lung Institute

Senior Teaching Fellow
 
 
 
//

Contact

 

+44 (0)20 7594 1980c.wiegman

 
 
//

Location

 

305Guy Scadding BuildingRoyal Brompton Campus

//

Summary

 

Publications

Citation

BibTex format

@article{Michaudel:2018:10.3389/fimmu.2018.00916,
author = {Michaudel, C and Maillet, I and Fauconnier, L and Quesniaux, V and Chung, KF and Wiegman, C and Peter, D and Ryffel, B},
doi = {10.3389/fimmu.2018.00916},
journal = {Frontiers in Immunology},
title = {Interleukin-1 alpha mediates ozone-induced myeloid differentiation factor-88-dependent epithelial tissue injury and inflammation},
url = {http://dx.doi.org/10.3389/fimmu.2018.00916},
volume = {9},
year = {2018}
}
Download

RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Air pollution associated with ozone exposure represents a major inducer of respiratory disease in man. In mice, a single ozone exposure causes lung injury with disruption of the respiratory barrier and inflammation. We investigated the role of interleukin-1 (IL-1)-associated cytokines upon a single ozone exposure (1 ppm for 1 h) using IL-1α-, IL-1β-, and IL-18-deficient mice or an anti-IL-1α neutralizing antibody underlying the rapid epithelial cell death. Here, we demonstrate the release of the alarmin IL-1α after ozone exposure and that the acute respiratory barrier injury and inflammation and airway hyperreactivity are IL-1α-dependent. IL-1α signaling via IL-1R1 depends on the adaptor protein myeloid differentiation factor-88 (MyD88). Importantly, epithelial cell signaling is critical, since deletion of MyD88 in lung type I alveolar epithelial cells reduced ozone-induced inflammation. In addition, intratracheal injection of recombinant rmIL-1α in MyD88acid mice led to reduction of inflammation in comparison with wild type mice treated with rmIL-1α. Therefore, a major part of inflammation is mediated by IL-1α signaling in epithelial cells. In conclusion, the alarmin IL-1α released upon ozone-induced tissue damage and inflammation is mediated by MyD88 signaling in epithelial cells. Therefore, IL-1α may represent a therapeutic target to attenuate ozone-induced lung inflammation and hyperreactivity.
AU  - Michaudel,C
AU  - Maillet,I
AU  - Fauconnier,L
AU  - Quesniaux,V
AU  - Chung,KF
AU  - Wiegman,C
AU  - Peter,D
AU  - Ryffel,B
DO  - 10.3389/fimmu.2018.00916
PY  - 2018///
SN  - 1664-3224
TI  - Interleukin-1 alpha mediates ozone-induced myeloid differentiation factor-88-dependent epithelial tissue injury and inflammation
T2  - Frontiers in Immunology
UR  - http://dx.doi.org/10.3389/fimmu.2018.00916
UR  - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000431502000001&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR  - http://hdl.handle.net/10044/1/60617
VL  - 9
ER  -
Download