{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T13:02:15Z","timestamp":1792155735615,"version":"4.4.0"},"reference-count":72,"publisher":"American Society for Clinical Investigation","issue":"4","license":[{"start":{"date-parts":[[2023,2,22]],"date-time":"2023-02-22T00:00:00Z","timestamp":1677024000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001711","name":"Swiss National Science Foundation","doi-asserted-by":"crossref","award":["FN 310030-156173"],"award-info":[{"award-number":["FN 310030-156173"]}],"id":[{"id":"10.13039\/501100001711","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100003186","name":"National Rosacea Society","doi-asserted-by":"crossref","award":["xxx"],"award-info":[{"award-number":["xxx"]}],"id":[{"id":"10.13039\/100003186","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Gottfried&Julia Bangerter-Rhyner foundation","award":["xxx"],"award-info":[{"award-number":["xxx"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2023,2,22]]},"abstract":"<jats:p>\n                    Rosacea is a common chronic inflammatory skin disease with a fluctuating course of excessive inflammation and apparent neovascularization. Microbial dysbiosis with a high density of\n                    <jats:italic>Bacillus<\/jats:italic>\n                    <jats:italic>oleronius<\/jats:italic>\n                    and increased activity of kallikrein 5, which cleaves cathelicidin antimicrobial peptide, are key pathogenic triggers in rosacea. However, how these events are linked to the disease remains unknown. Here, we show that type I IFNs produced by plasmacytoid DCs represent the pivotal link between dysbiosis, the aberrant immune response, and neovascularization. Compared with other commensal bacteria,\n                    <jats:italic>B<\/jats:italic>\n                    .\n                    <jats:italic>oleronius<\/jats:italic>\n                    is highly susceptible and preferentially killed by cathelicidin antimicrobial peptides, leading to enhanced generation of complexes with bacterial DNA. These bacterial DNA complexes but not DNA complexes derived from host cells are required for cathelicidin-induced activation of plasmacytoid DCs and type I IFN production. Moreover, kallikrein 5 cleaves cathelicidin into peptides with heightened DNA binding and type I IFN\u2013inducing capacities. In turn, excessive type I IFN expression drives neoangiogenesis via IL-22 induction and upregulation of the IL-22 receptor on endothelial cells. These findings unravel a potentially novel pathomechanism that directly links hallmarks of rosacea to the killing of dysbiotic commensal bacteria with induction of a pathogenic type I IFN\u2013driven and IL-22\u2013mediated angiogenesis.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.151846","type":"journal-article","created":{"date-parts":[[2023,1,12]],"date-time":"2023-01-12T12:00:36Z","timestamp":1673524836000},"source":"Crossref","is-referenced-by-count":29,"title":["Type I IFNs link skin-associated dysbiotic commensal bacteria to pathogenic inflammation and angiogenesis in rosacea"],"prefix":"10.1172","volume":"8","author":[{"given":"Alessio","family":"Mylonas","sequence":"first","affiliation":[{"name":"Department of Dermatology, University Hospital CHUV, Lausanne, Switzerland."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3990-8230","authenticated-orcid":true,"given":"Heike 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