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We used a severe psoriasis mouse model of keratinocyte IL\u201017A overexpression (K14\u2010IL\u201017A<jats:sup>ind\/+<\/jats:sup>, IL\u201017A<jats:sup>ind\/+<\/jats:sup> control mice) to investigate the activity of neutrophils and a potential cellular interconnection between skin and vasculature. Levels of dermal reactive oxygen species (ROS) and their release by neutrophils were measured by lucigenin\u2010\/luminol\u2010based assays, respectively. Quantitative RT\u2010PCR determined neutrophilic activity and inflammation\u2010related markers in skin and aorta. To track skin\u2010derived immune cells, we used PhAM\u2010K14\u2010IL\u201017A<jats:sup>ind\/+<\/jats:sup> mice allowing us to mark all cells in the skin by photoconversion of a fluorescent protein to analyze their migration into spleen, aorta, and lymph nodes by flow cytometry. Compared to controls, K14\u2010IL\u201017A<jats:sup>ind\/+<\/jats:sup> mice exhibited elevated ROS levels in the skin and a higher neutrophilic oxidative burst accompanied by the upregulation of several activation markers. In line with these results psoriatic mice displayed elevated expression of genes involved in neutrophil migration (e.g., <jats:italic>Cxcl2<\/jats:italic> and <jats:italic>S100a9<\/jats:italic>) in skin and aorta. However, no direct immune cell migration from the psoriatic skin into the aortic vessel wall was observed. Neutrophils of psoriatic mice showed an activated phenotype, but no direct cellular migration from the skin to the vasculature was observed. This suggests that highly active vasculature\u2010invading neutrophils must originate directly from the bone marrow. Hence, the skin\u2010vasculature crosstalk in psoriasis is most likely based on the systemic effects of the autoimmune skin disease, emphasizing the importance of a systemic therapeutic approach for psoriasis patients.<\/jats:p>","DOI":"10.1002\/biof.1949","type":"journal-article","created":{"date-parts":[[2023,5,4]],"date-time":"2023-05-04T08:41:03Z","timestamp":1683189663000},"page":"861-874","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Reactive oxygen species produced by myeloid cells in psoriasis as a potential biofactor contributing to the development of vascular inflammation"],"prefix":"10.1002","volume":"49","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1208-7823","authenticated-orcid":false,"given":"Theresa","family":"Schaller","sequence":"first","affiliation":[{"name":"Institute for Molecular Medicine University Medical Center of the Johannes Gutenberg\u2010University Mainz  Mainz 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Gutenberg\u2010University Mainz  Mainz Germany"},{"name":"Department of Hematology and Central Hematology Laboratory Inselspital University Hospital Bern  Bern Switzerland"},{"name":"Department of Clinical Research University of Bern  Bern Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2428-2658","authenticated-orcid":false,"given":"Katharina S.","family":"Kommoss","sequence":"additional","affiliation":[{"name":"Division of Chronic Inflammation and Cancer German Cancer Research Center (DKFZ)  Heidelberg Germany"},{"name":"Department of Dermatology University of Heidelberg  Heidelberg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"Korn","sequence":"additional","affiliation":[{"name":"Institute for Experimental Neuroimmunology Technical University of Munich School of Medicine  Munich Germany"},{"name":"Munich Cluster for Systems Neurology (SyNergy) 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