Imperial College London
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ProfessorCeciliaJohansson

Faculty of Medicine, National Heart & Lung Institute

Professor of Mucosal Immunology
 
 
 
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Contact

 

+44 (0)20 7594 2531c.johansson

 
 
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Location

 

367Wright Fleming WingSt Mary's Campus

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Summary

 

Publications

Citation

BibTex format

@article{Goritzka:2014:10.1128/JVI.00333-14,
author = {Goritzka, M and Durant, LR and Pereira, C and Salek-Ardakani, S and Openshaw, PJM and Johansson, C},
doi = {10.1128/JVI.00333-14},
journal = {Journal of Virology},
pages = {6128--6136},
title = {Alpha/Beta Interferon Receptor Signaling Amplifies Early Proinflammatory Cytokine Production in the Lung during Respiratory Syncytial Virus Infection},
url = {http://dx.doi.org/10.1128/JVI.00333-14},
volume = {88},
year = {2014}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Type I interferons (IFNs) are produced early upon virus infection and signal through the alpha/beta interferon (IFN-α/β) receptor (IFNAR) to induce genes that encode proteins important for limiting viral replication and directing immune responses. To investigate the extent to which type I IFNs play a role in the local regulation of inflammation in the airways, we examined their importance in early lung responses to infection with respiratory syncytial virus (RSV). IFNAR1-deficient (IFNAR1−/−) mice displayed increased lung viral load and weight loss during RSV infection. As expected, expression of IFN-inducible genes was markedly reduced in the lungs of IFNAR1−/− mice. Surprisingly, we found that the levels of proinflammatory cytokines and chemokines in the lungs of RSV-infected mice were also greatly reduced in the absence of IFNAR signaling. Furthermore, low levels of proinflammatory cytokines were also detected in the lungs of IFNAR1−/− mice challenged with noninfectious innate immune stimuli such as selected Toll-like receptor (TLR) agonists. Finally, recombinant IFN-α was sufficient to potentiate the production of inflammatory mediators in the lungs of wild-type mice challenged with innate immune stimuli. Thus, in addition to its well-known role in antiviral resistance, type I IFN receptor signaling acts as a central driver of early proinflammatory responses in the lung. Inhibiting the effects of type I IFNs may therefore be useful in dampening inflammation in lung diseases characterized by enhanced inflammatory cytokine production.
AU  - Goritzka,M
AU  - Durant,LR
AU  - Pereira,C
AU  - Salek-Ardakani,S
AU  - Openshaw,PJM
AU  - Johansson,C
DO  - 10.1128/JVI.00333-14
EP  - 6136
PY  - 2014///
SN  - 0022-538X
SP  - 6128
TI  - Alpha/Beta Interferon Receptor Signaling Amplifies Early Proinflammatory Cytokine Production in the Lung during Respiratory Syncytial Virus Infection
T2  - Journal of Virology
UR  - http://dx.doi.org/10.1128/JVI.00333-14
UR  - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000335970300021&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR  - https://jvi.asm.org/content/88/11/6128/
UR  - http://hdl.handle.net/10044/1/19051
VL  - 88
ER  -
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