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Thus, restoring levels of specialized pro\u2010resolving mediators (SPMs) to promote the resolution of inflammation has been proposed as a therapeutic strategy for patients with atherosclerosis, in addition to standard clinical care. Herein, we evaluated the effects of the SPM lipids, lipoxin A\n                    <jats:sub>4<\/jats:sub>\n                    (LXA\n                    <jats:sub>4<\/jats:sub>\n                    ) and lipoxin B\n                    <jats:sub>4<\/jats:sub>\n                    (LXB\n                    <jats:sub>4<\/jats:sub>\n                    ), on neutrophils isolated from patients with atherosclerosis compared with healthy controls. Patients displayed altered endogenous SPM production, and we demonstrated that lipoxin treatment in whole blood from atherosclerosis patients attenuates neutrophil oxidative burst, a key contributor to atherosclerotic development. We found the opposite effect in neutrophils from healthy controls, indicating a potential mechanism whereby lipoxins aid the endogenous neutrophil function in health but reduce its excessive activation in disease. We also demonstrated that lipoxins attenuated upregulation of the high\u2010affinity conformation of the CD11b\/CD18 integrin, which plays a central role in clot activation and atherosclerosis. Finally, LXB\n                    <jats:sub>4<\/jats:sub>\n                    enhanced lymphatic transmigration of human neutrophils isolated from patients with atherosclerosis. This finding is noteworthy, as impaired lymphatic function is now recognized as an important contributor to atherosclerosis. Although both lipoxins modulated neutrophil function, LXB\n                    <jats:sub>4<\/jats:sub>\n                    displayed more potent effects than LXA\n                    <jats:sub>4<\/jats:sub>\n                    in humans. This study highlights the therapeutic potential of lipoxins in atherosclerotic disease and demonstrates that the effect of these SPMs may be specifically tailored to the need of the individual.\n                  <\/jats:p>","DOI":"10.1096\/fj.202101219rr","type":"journal-article","created":{"date-parts":[[2022,2,1]],"date-time":"2022-02-01T09:46:25Z","timestamp":1643708785000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":28,"title":["Lipoxins modulate neutrophil oxidative burst, integrin expression and lymphatic transmigration differentially in human health and atherosclerosis"],"prefix":"10.1096","volume":"36","author":[{"given":"Jamie D.","family":"Kraft","sequence":"first","affiliation":[{"name":"Department of Molecular and Clinical Medicine Wallenberg Laboratory Institute of Medicine Sahlgrenska Academy University of Gothenburg  Gothenburg Sweden"},{"name":"Wallenberg Centre for Molecular and Translational Medicine 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Clinical Physiology Region Vaestra Goetaland Sahlgrenska University Hospital  Gothenburg Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6328-3640","authenticated-orcid":false,"given":"Jesmond","family":"Dalli","sequence":"additional","affiliation":[{"name":"William Harvey Research Institute Barts &amp; The London School of Medicine &amp; Dentistry Queen Mary University of London  London UK"},{"name":"Centre for Inflammation and Therapeutic Innovation Queen Mary University of London  London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sofia","family":"Nystr\u00f6m","sequence":"additional","affiliation":[{"name":"Department of Clinical Immunology and Transfusion Medicine Link\u00f6ping University  Link\u00f6ping Sweden"},{"name":"Department of Biomedical and Clinical Sciences Link\u00f6ping University  Link\u00f6ping 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