BibTex format
@article{Katsoulis:2024:10.1038/s41467-024-50197-0,
author = {Katsoulis, O and Toussaint, M and Jackson, M and Mallia, P and Footitt, J and Mincham, K and Meyer, G and Kebadze, T and Gilmour, A and Long, M and Aswani, A and Snelgrove, R and Johnston, S and Chalmers, J and Singanayagam, A},
doi = {10.1038/s41467-024-50197-0},
journal = {Nature Communications},
title = {Neutrophil extracellular traps promote immunopathogenesis of virus-induced COPD exacerbations},
url = {http://dx.doi.org/10.1038/s41467-024-50197-0},
volume = {15},
year = {2024}
}
RIS format (EndNote, RefMan)
TY - JOUR
AB - Respiratory viruses are a major trigger of exacerbations in chronic obstructive pulmonary disease (COPD). Airway neutrophilia is a hallmark feature of stable and exacerbated COPD but roles played by neutrophil extracellular traps (NETS) in driving disease pathogenesis are unclear. Here, using human studies of experimentally-induced and naturally-occurring exacerbations we identify that rhinovirus infection induces airway NET formation which is amplified in COPD and correlates with magnitude of inflammation and clinical exacerbation severity. We show that inhibiting NETosis protects mice from immunopathology in a model of virus-exacerbated COPD. NETs drive inflammation during exacerbations through release of double stranded DNA (dsDNA) and administration of DNAse in mice has similar protective effects. Thus, NETosis, through release of dsDNA, has a functional role in the pathogenesis of COPD exacerbations. These studies open up the potential for therapeutic targeting of NETs or dsDNA as a strategy for treating virus-exacerbated COPD.
AU - Katsoulis,O
AU - Toussaint,M
AU - Jackson,M
AU - Mallia,P
AU - Footitt,J
AU - Mincham,K
AU - Meyer,G
AU - Kebadze,T
AU - Gilmour,A
AU - Long,M
AU - Aswani,A
AU - Snelgrove,R
AU - Johnston,S
AU - Chalmers,J
AU - Singanayagam,A
DO - 10.1038/s41467-024-50197-0
PY - 2024///
SN - 2041-1723
TI - Neutrophil extracellular traps promote immunopathogenesis of virus-induced COPD exacerbations
T2 - Nature Communications
UR - http://dx.doi.org/10.1038/s41467-024-50197-0
UR - https://www.nature.com/articles/s41467-024-50197-0
UR - http://hdl.handle.net/10044/1/112918
VL - 15
ER -