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However, detailed knowledge regarding the role of complement in<jats:named-content content-type=\"genus-species\">Staphylococcus aureus<\/jats:named-content>septic arthritis is still largely missing. In this study, we elucidated the roles of selected complement proteins in<jats:named-content content-type=\"genus-species\">S. aureus<\/jats:named-content>septic arthritis. Mice lacking the complement component 3 (<jats:italic>C3<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>), complement factor B (<jats:italic>fB<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>), and receptor for C3-derived anaphylatoxin C3a (<jats:italic>C3aR<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>) and wild-type (WT) control mice were intravenously or intra-articularly inoculated with<jats:named-content content-type=\"genus-species\">S. aureus<\/jats:named-content>strain Newman. The clinical course of septic arthritis, as well as histopathological and radiological changes in joints, was assessed. After intravenous inoculation, arthritis severity and frequency were significantly higher in<jats:italic>C3<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>mice than in WT controls, whereas<jats:italic>fB<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>mice displayed intermediate arthritis severity and frequency. This was in accordance with both histopathological and radiological findings. C3, but not fB, deficiency was associated with greater weight loss, more frequent kidney abscesses, and higher bacterial burden in kidneys.<jats:named-content content-type=\"genus-species\">S. aureus<\/jats:named-content>opsonized with<jats:italic>C3<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>sera displayed decreased uptake by mouse peritoneal macrophages compared with bacteria opsonized with WT or<jats:italic>fB<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>sera. C3aR deficiency had no effect on the course of hematogenous<jats:named-content content-type=\"genus-species\">S. aureus<\/jats:named-content>septic arthritis. We conclude that C3 deficiency increases susceptibility to hematogenous<jats:named-content content-type=\"genus-species\">S. aureus<\/jats:named-content>septic arthritis and impairs host bacterial clearance, conceivably due to diminished opsonization and phagocytosis of<jats:named-content content-type=\"genus-species\">S. aureus<\/jats:named-content>.<\/jats:p>","DOI":"10.1128\/iai.01520-15","type":"journal-article","created":{"date-parts":[[2016,1,20]],"date-time":"2016-01-20T03:58:49Z","timestamp":1453262329000},"page":"930-939","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":37,"title":["Deficiency of the Complement Component 3 but Not Factor B Aggravates Staphylococcus aureus Septic Arthritis in Mice"],"prefix":"10.1128","volume":"84","author":[{"given":"Manli","family":"Na","sequence":"first","affiliation":[{"name":"Department of Rheumatology and Inflammation Research, Institution of Medicine, Sahlgrenska 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