Imperial College London
Dr Carmel Stock

DrCarmelStock

Faculty of Medicine, National Heart & Lung Institute

Honorary Research Associate
 
 
 
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Contact

 

c.stock

 
 
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Location

 

2129Sydney StreetRoyal Brompton Campus

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Summary

 

Publications

Citation

BibTex format

@article{Molyneaux:2017:10.1164/rccm.201607-1408OC,
author = {Molyneaux, PL and Willis, Owen SA and Cox, MJ and James, P and Cowman, S and Loebinger, M and Blanchard, A and Edwards, LM and Stock, C and Daccord, C and Renzoni, EA and Wells, AU and Moffatt, MF and Cookson, WO and Maher, TM},
doi = {10.1164/rccm.201607-1408OC},
journal = {American Journal of Respiratory and Critical Care Medicine},
pages = {1640--1650},
title = {Host-microbial interactions in idiopathic pulmonary fibrosis},
url = {http://dx.doi.org/10.1164/rccm.201607-1408OC},
volume = {195},
year = {2017}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - RATIONALE: Changes in the respiratory microbiome are associated with disease progression in Idiopathic pulmonary fibrosis (IPF). The role of the host response to the respiratory microbiome however remains unknown. OBJECTIVES: To explore the host-microbial interaction in IPF. METHODS: Sixty patients diagnosed with IPF were prospectively enrolled, together with 20 matched controls. Subjects underwent bronchoalveolar lavage (BAL) and peripheral whole blood was collected into PAXgene tubes for all subjects at baseline. For IPF subjects additional samples were taken at 1, 3, and 6 months and (if alive) a year. Gene expression profiles were generated using Affymetrix Human Gene1.1ST Arrays. MEASUREMENTS AND MAIN RESULTS: Network analysis of gene expression data identified two gene modules that strongly associate with a diagnosis of IPF, BAL bacterial burden (determined by 16S quantitative PCR) and specific microbial OTUs, as well as lavage and peripheral blood neutrophilia. Genes within these modules that are involved in the host defence response include NLRC4, PGLYRP1, MMP9, DEFA4. The modules also contain two genes encoding specific antimicrobial peptides (SLPI and CAMP). Many of these particular transcripts were associated with survival and showed longitudinal over expression in subjects experiencing disease progression, further strengthening their relationship with disease. CONCLUSIONS: Integrated analysis of the host transcriptome and microbial signatures demonstrates an apparent host response to the presence of an altered or more abundant microbiome. These responses remain elevated on longitudinal follow up, suggesting that the bacterial communities of the lower airways may be acting as persistent stimuli for repetitive alveolar injury in IPF.
AU  - Molyneaux,PL
AU  - Willis,Owen SA
AU  - Cox,MJ
AU  - James,P
AU  - Cowman,S
AU  - Loebinger,M
AU  - Blanchard,A
AU  - Edwards,LM
AU  - Stock,C
AU  - Daccord,C
AU  - Renzoni,EA
AU  - Wells,AU
AU  - Moffatt,MF
AU  - Cookson,WO
AU  - Maher,TM
DO  - 10.1164/rccm.201607-1408OC
EP  - 1650
PY  - 2017///
SN  - 1535-4970
SP  - 1640
TI  - Host-microbial interactions in idiopathic pulmonary fibrosis
T2  - American Journal of Respiratory and Critical Care Medicine
UR  - http://dx.doi.org/10.1164/rccm.201607-1408OC
UR  - http://www.ncbi.nlm.nih.gov/pubmed/28085486
UR  - https://www.atsjournals.org/doi/10.1164/rccm.201607-1408OC
UR  - http://hdl.handle.net/10044/1/44257
VL  - 195
ER  -
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