[摘要]：Methods. Mice were intravenously inoculated with wild-type S. aureus strain RN4220 or its isogenic mutant strain (delta fmt) lacking the ability to produce formylated peptides. The development of arthritis was followed clinically and histopathologically. Results. Mice inoculated with the formyl peptide-producing wild-type strain showed a significantly increased frequency and severity of arthritis and subsequent joint destruction as compared with delta fmt mutant strain-inoculated mice. The wild-type S. aureus strain also induced significantly more weight loss than the delta fmt mutant strain. The recruitment of neutrophils into infected kidneys and synovial tissue was significantly higher in mice inoculated with the wild-type strain. Conclusions. Our data show that formylated peptides function as important virulence factors in S. aureus arthritis, partly by mediating neutrophil recruitment, which contributes substantially to the joint damage.
