As is the case in the pathogenesis of osteomyelitis, S. aureus MSCRAMMs mediate adherence to host proteins in the joint extracellular matrix, a process that is more likely to occur in damaged or healing joints (463). Upon seeding the synovial membrane, bacteria pass into the joint space. Synovial fluid inhibits S. aureus growth in vitro (464), an observation that is at odds with the substantial damage caused by S. aureus septic arthritis. Several avenues of investigation have clarified this apparent contradiction. In murine models, there is a rapid recruitment of neutrophils, mediated by formylated peptides (465), after S. aureus gains entry to the joint space. Activated macrophages and T cells are recruited as well, and a host of cytokines are induced, including tumor necrosis factor alpha (TNF-α), gamma interferon (IFN-γ), interleukin-1 (IL-1), IL-2, IL-6, and IL-17 (466). Neutrophils, however, play a dual role. They are needed for bacterial clearance, and their absence in experimental models leads to higher mortality rates and worse arthritis (467); however, they also contribute to tissue damage via enzyme release and free radical formation. A study of human synovial fluid also demonstrated that S. aureus forms large aggregates with host-derived fibrin, a finding that suggests a possible explanation for in vivo resistance to killing by neutrophils, as these aggregates are too large for neutrophil phagocytosis (468).
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