Neutrophil extracellular traps promote immunopathogenesis of virus-induced COPD exacerbations

Orestis Katsoulis, Marie Toussaint, Millie M. Jackson, Patrick Mallia, Joseph Footitt, Kyle T. Mincham, Garance F. M. Meyer, Tata Kebadze, Amy Gilmour, Merete Long, Andrew D. Aswani, Robert J. Snelgrove, Sebastian L. Johnston, James D. Chalmers and Aran Singanayagam ()
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Orestis Katsoulis: Imperial College London
Marie Toussaint: Imperial College London
Millie M. Jackson: Imperial College London
Patrick Mallia: Imperial College London
Joseph Footitt: Imperial College London
Kyle T. Mincham: Imperial College London
Garance F. M. Meyer: Imperial College London
Tata Kebadze: Imperial College London
Amy Gilmour: Ninewells Hospital and Medical School
Merete Long: Ninewells Hospital and Medical School
Andrew D. Aswani: Guy’s and St Thomas’ NHS Foundation Trust
Robert J. Snelgrove: Imperial College London
Sebastian L. Johnston: Imperial College London
James D. Chalmers: Ninewells Hospital and Medical School
Aran Singanayagam: Imperial College London

Nature Communications, 2024, vol. 15, issue 1, 1-14

Abstract: Abstract 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.

Date: 2024
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DOI: 10.1038/s41467-024-50197-0

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