Imperial College London
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Peter Openshaw - Professor of Experimental Medicine

Faculty of Medicine, National Heart & Lung Institute

Proconsul, Professor of Experimental Medicine
 
 
 
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Contact

 

+44 (0)20 7594 3854p.openshaw Website CV

 
 
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Assistant

 

Ms Gale Lewis +44 (0)20 7594 0944

 
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Location

 

353Norfolk PlaceSt Mary's Campus

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Summary

 

Publications

Citation

BibTex format

@article{Thwaites:2018:10.1164/rccm.201712-2567OC,
author = {Thwaites, RS and Coates, M and Ito, K and Ghazaly, M and Feather, C and Abdulla, F and Tunstall, T and Jain, P and Cass, L and Rapeport, G and Hansel, TT and Nadel, S and Openshaw, PJ},
doi = {10.1164/rccm.201712-2567OC},
journal = {American Journal of Respiratory and Critical Care Medicine},
pages = {1074--1084},
title = {Reduced nasal viral load and IFN responses in infants with RSV bronchiolitis and respiratory failure},
url = {http://dx.doi.org/10.1164/rccm.201712-2567OC},
volume = {198},
year = {2018}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - RATIONALE: Respiratory syncytial virus (RSV) bronchiolitis is a major cause of morbidity and mortality in infancy. Severe disease is thought to result from uncontrolled viral replication, an excessive immune response, or both. OBJECTIVES: To determine RSV load and immune mediator levels in nasal mucosal lining fluid by serial sampling of nasal fluids from cases of moderate and severe bronchiolitis over the course of infection. METHODS: Infants with viral bronchiolitis necessitating admission (n=55) were recruited from a paediatric centre during 2016/17. Of these, 30 were RSV infected (18 'moderate', and 12 mechanically ventilated 'severe'). Nasal fluids were sampled frequently over time using nasosorption devices and nasophayngeal aspiration (NPA). Hierarchical clustering of time weighted averages (TWA) was performed to investigate cytokine and chemokine levels, and gene expression profiling was conducted. MEASUREMENTS AND MAIN RESULTS: Unexpectedly, cases of severe RSV bronchiolitis had lower nasal viral loads and reduced interferon (IFN)-γ and CCL5/RANTES levels compared to those with moderate disease, especially when allowance was made for disease duration (all P<0.05). Reduced cytokine/chemokine levels in severe disease were also seen in children with other viral infections. Gene expression analysis of NPA samples (n=43) confirmed reduced type-I IFN gene expression in severe bronchiolitis accompanied by enhanced expression of MUC5AC and IL17A. CONCLUSIONS: Infants with severe RSV bronchiolitis have lower nasal viral load, IP-10/CXCL10 and type-I IFNs levels compared to moderately ill children, but enhanced MUC5AC and IL17A gene expression in nasal cells.
AU  - Thwaites,RS
AU  - Coates,M
AU  - Ito,K
AU  - Ghazaly,M
AU  - Feather,C
AU  - Abdulla,F
AU  - Tunstall,T
AU  - Jain,P
AU  - Cass,L
AU  - Rapeport,G
AU  - Hansel,TT
AU  - Nadel,S
AU  - Openshaw,PJ
DO  - 10.1164/rccm.201712-2567OC
EP  - 1084
PY  - 2018///
SN  - 1073-449X
SP  - 1074
TI  - Reduced nasal viral load and IFN responses in infants with RSV bronchiolitis and respiratory failure
T2  - American Journal of Respiratory and Critical Care Medicine
UR  - http://dx.doi.org/10.1164/rccm.201712-2567OC
UR  - https://www.ncbi.nlm.nih.gov/pubmed/29688024
UR  - https://www.atsjournals.org/doi/10.1164/rccm.201712-2567OC
UR  - http://hdl.handle.net/10044/1/60334
VL  - 198
ER  -
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