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Candidalysin is critical for mucosal C albicans infections and is known to activate epithelial cells to induce downstream innate immune responses that are associated with protection or immunopathology during oral or vaginal infections. Furthermore, candidalysin activates the NLRP3 inflammasome and causes cytolysis in mononuclear phagocytes. However, the role of candidalysin in driving systemic infections is unknown.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>In this study, using candidalysin-producing and candidalysin-deficient C albicans strains, we show that candidalysin activates mitogen-activated protein kinase (MAPK) signaling and chemokine secretion in endothelial cells in vitro.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Candidalysin induces immune activation and neutrophil recruitment in vivo, and it promotes mortality in zebrafish and murine models of systemic fungal infection.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>The data demonstrate a key role for candidalysin in neutrophil recruitment and fungal virulence during disseminated systemic C albicans infections.<\/jats:p><\/jats:sec>","DOI":"10.1093\/infdis\/jiz322","type":"journal-article","created":{"date-parts":[[2019,7,1]],"date-time":"2019-07-01T19:10:09Z","timestamp":1562008209000},"page":"1477-1488","source":"Crossref","is-referenced-by-count":116,"title":["Candidalysin Is Required for Neutrophil Recruitment and Virulence During Systemic Candida albicans Infection"],"prefix":"10.1093","volume":"220","author":[{"given":"Marc","family":"Swidergall","sequence":"first","affiliation":[{"name":"Division of Infectious Diseases, Harbor-UCLA Medical Center, Torrance, California"},{"name":"Institute for Infection and Immunity, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mina","family":"Khalaji","sequence":"additional","affiliation":[{"name":"School of Clinical Dentistry, Claremont Crescent, University of Sheffield, United Kingdom"},{"name":"Present Affiliation: Department 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and Infectious Diseases, National Institutes of Health, Bethesda, Maryland"},{"name":"Present Affiliation: Institute of Immunology and Immunotherapy, Institute of Microbiology and Infection, University of Birmingham, Edgbaston, Birmingham, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bernhard","family":"Hube","sequence":"additional","affiliation":[{"name":"Department of Microbial Pathogenicity Mechanisms, Leibniz Institute for Natural Product Research and Infection Biology (Hans Knoell Institute), Jena, Germany"},{"name":"Friedrich Schiller University, Jena, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michail S","family":"Lionakis","sequence":"additional","affiliation":[{"name":"Fungal Pathogenesis Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, 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