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COPD is associated with persistent blood and airway neutrophilia and systemic and tissue hypoxia. Hypoxia augments neutrophil elastase release, enhancing capacity for tissue injury.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>To determine whether hypoxia-driven neutrophil protein secretion contributes to endothelial damage in COPD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>The healthy human neutrophil secretome generated under normoxic or hypoxic conditions was characterized by quantitative mass spectrometry, and the capacity for neutrophil-mediated endothelial damage was assessed. Histotoxic protein concentrations were measured in normoxic versus hypoxic neutrophil supernatants and plasma from patients experiencing COPD exacerbation and healthy control subjects.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>Hypoxia promoted PI3K\u03b3-dependent neutrophil elastase secretion, with greater release seen in neutrophils from patients with COPD. Supernatants from neutrophils incubated under hypoxia caused pulmonary endothelial cell damage, and identical supernatants from COPD neutrophils increased neutrophil adherence to endothelial cells. Proteomics revealed differential neutrophil protein secretion under hypoxia and normoxia, and hypoxia augmented secretion of a subset of histotoxic granule and cytosolic proteins, with significantly greater release seen in COPD neutrophils. The plasma of patients with COPD had higher content of hypoxia-upregulated neutrophil-derived proteins and protease activity, and vascular injury markers.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Hypoxia drives a destructive \u201chypersecretory\u201d neutrophil phenotype conferring enhanced capacity for endothelial injury, with a corresponding signature of neutrophil degranulation and vascular injury identified in plasma of patients with COPD. Thus, hypoxic enhancement of neutrophil degranulation may contribute to increased cardiovascular risk in COPD. These insights may identify new therapeutic opportunities for endothelial damage in COPD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1164\/rccm.202006-2467oc","type":"journal-article","created":{"date-parts":[[2022,1,19]],"date-time":"2022-01-19T16:04:23Z","timestamp":1642608263000},"page":"903-916","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":89,"title":["Hypoxia Increases the Potential for Neutrophil-mediated Endothelial Damage in Chronic Obstructive Pulmonary Disease"],"prefix":"10.1093","volume":"205","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3203-9941","authenticated-orcid":false,"given":"Katharine M.","family":"Lodge","sequence":"first","affiliation":[{"name":"Department of Medicine, School of Clinical Medicine, University of Cambridge, Cambridge, United Kingdom"},{"name":"National Heart and Lung Institute, Imperial College London, London, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Arlette","family":"Vassallo","sequence":"additional","affiliation":[{"name":"Department of Medicine, School of Clinical Medicine, University of Cambridge, Cambridge, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bin","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Medicine, School of Clinical Medicine, University of Cambridge, Cambridge, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Merete","family":"Long","sequence":"additional","affiliation":[{"name":"Department of Infection, Immunity, and Cardiovascular Disease, University of Sheffield, Sheffield, United Kingdom; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhen","family":"Tong","sequence":"additional","affiliation":[{"name":"Department of Medicine, School of Clinical Medicine, University of Cambridge, Cambridge, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul R.","family":"Newby","sequence":"additional","affiliation":[{"name":"Institute of Inflammation and Ageing, University of Birmingham and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Danya","family":"Agha-Jaffar","sequence":"additional","affiliation":[{"name":"National Heart and Lung Institute, Imperial College London, London, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Koralia","family":"Paschalaki","sequence":"additional","affiliation":[{"name":"National Heart and Lung Institute, Imperial College London, London, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Clara E.","family":"Green","sequence":"additional","affiliation":[{"name":"Institute of Inflammation and Ageing, University of Birmingham and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kylie B. 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