Deficiency of the Complement Component 3 but Not Factor B Aggravates Staphylococcus aureus Septic Arthritis in Mice.

The complement system plays an essential role in the innate immune response and protection against bacterial infections. However, detailed knowledge regarding the role of complement inStaphylococcus aureusseptic arthritis is still largely missing. In this study, we elucidated the roles of selected complement proteins inS. aureusseptic arthritis. Mice lacking the complement component 3 (C3(-/-)), complement factor B (fB(-/-)), and receptor for C3-derived anaphylatoxin C3a (C3aR(-/-)) and wild-type (WT) control mice were intravenously or intra-articularly inoculated withS. aureusstrain 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 inC3(-/-)mice than in WT controls, whereasfB(-/-)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.S. aureusopsonized withC3(-/-)sera displayed decreased uptake by mouse peritoneal macrophages compared with bacteria opsonized with WT orfB(-/-)sera. C3aR deficiency had no effect on the course of hematogenousS. aureusseptic arthritis. We conclude that C3 deficiency increases susceptibility to hematogenousS. aureusseptic arthritis and impairs host bacterial clearance, conceivably due to diminished opsonization and phagocytosis ofS. aureus.

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