Imperial College London
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ProfessorRobertSnelgrove

Faculty of Medicine, National Heart & Lung Institute

Professor of Respiratory Science
 
 
 
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Contact

 

+44 (0)20 7594 8192robert.snelgrove

 
 
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Location

 

Sir Alexander Fleming BuildingSouth Kensington Campus

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Summary

 

Publications

Citation

BibTex format

@article{Snelgrove:2015:10.1038/ncomms9423,
author = {Snelgrove, RJ},
doi = {10.1038/ncomms9423},
journal = {Nature Communications},
pages = {1--14},
title = {Matrikines are key regulators in modulating the amplitude of lung inflammation in acute pulmonary infection},
url = {http://dx.doi.org/10.1038/ncomms9423},
volume = {6},
year = {2015}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Bioactive matrix fragments (matrikines) have been identified in a myriad of disorders, but their impact on the evolution of airway inflammation has not been demonstrated. We recently described a pathway where the matrikine and neutrophil chemoattractant proline–glycine–proline (PGP) could be degraded by the enzyme leukotriene A4 hydrolase (LTA4H). LTA4H classically functions in the generation of pro-inflammatory leukotriene B4, thus LTA4H exhibits opposing pro- and anti-inflammatory activities. The physiological significance of this secondary anti-inflammatory activity remains unknown. Here we show, using readily resolving pulmonary inflammation models, that loss of this secondary activity leads to more pronounced and sustained inflammation and illness owing to PGP accumulation. PGP elicits an exacerbated neutrophilic inflammation and protease imbalance that further degrades the extracellular matrix, generating fragments that perpetuate inflammation. This highlights a critical role for the secondary anti-inflammatory activity of LTA4H and thus has consequences for the generation of global LTA4H inhibitors currently being developed.
AU  - Snelgrove,RJ
DO  - 10.1038/ncomms9423
EP  - 14
PY  - 2015///
SN  - 2041-1723
SP  - 1
TI  - Matrikines are key regulators in modulating the amplitude of lung inflammation in acute pulmonary infection
T2  - Nature Communications
UR  - http://dx.doi.org/10.1038/ncomms9423
UR  - https://www.nature.com/articles/ncomms9423
UR  - http://hdl.handle.net/10044/1/26009
VL  - 6
ER  -
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