Abstract
BackgroundStaphylococcus aureus is the most common agent of septic arthritis that is a severe, rapidly progressive and destructive joint disease. Superantigens produced by S. aureus are considered the major arthritogenic factors. In this study, we compared the arthritogenic potential of five superantigen-producing staphylococcal strains.MethodsMale C57BL/6 mice were intravenously infected with ATCC 19095 SEC+, N315 ST5 TSST-1+, S-70 TSST-1+, ATCC 51650 TSST-1+ and ATCC 13565 SEA+ strains. Clinical parameters as body weight, arthritis incidence and clinical score were daily evaluated. Joint histopathological analysis and spleen cytokine production were evaluated at the 14th day after infection.ResultsWeight loss was observed in all infected mice. ATCC 19095 SEC+, N315 ST5 TSST-1+ and S-70 TSST-1+ were arthritogenic, being the highest scores observed in ATCC 19095 SEC+ infected mice. Intermediate and lower clinical scores were observed in N315 ST5 TSST-1+ and S-70 TSST-1+ infected mice, respectively. The ATCC 13565 SEA+ strain caused death of 85% of the animals after 48 h. Arthritis triggered by the ATCC 19095 SEC+ strain was characterized by accentuated synovial hyperplasia, inflammation, pannus formation, cartilage destruction and bone erosion. Similar joint alterations were found in N315 ST5 TSST-1+ infected mice, however they were strikingly more discrete. Only minor synovial proliferation and inflammation were triggered by the S-70 TSST-1+ strain. The lowest levels of TNF-α, IL-6 and IL-17 production in response to S. aureus stimulation were found in cultures from mice infected with the less arthritogenic strains (S-70 TSST-1+ and ATCC 51650 TSST-1+). The highest production of IL-17 was detected in mice infected with the most arthritogenic strains (ATCC 19095 SEC+ and N315 ST5 TSST-1+).ConclusionsTogether these results demonstrated that S. aureus strains, isolated from biological samples, were able to induce a typical septic arthritis in mice. These results also suggest that the variable arthritogenicity of these strains was, at least in part, related to their differential ability to induce IL-17 production.
Highlights
Staphylococcus aureus is the most common agent of septic arthritis that is a severe, rapidly progressive and destructive joint disease
Staphylococcus aureus is a major cause of bacteremia which frequently leads to infective endocarditis, metastatic abscess formation, toxic shock syndrome, gastroenteritis, pneumonia, osteomyelitis and septic arthritis (SA) [1]
Arthritis incidence The kinetics of arthritis development was very similar in the groups infected with American type culture collection (ATCC) 19095 Staphylococcal enterotoxin C (SEC)+ and N315 ST5 Toxic shock syndrome toxin (TSST)-1+
Summary
Staphylococcus aureus is the most common agent of septic arthritis that is a severe, rapidly progressive and destructive joint disease. Staphylococcus aureus is a major cause of bacteremia which frequently leads to infective endocarditis, metastatic abscess formation, toxic shock syndrome, gastroenteritis, pneumonia, osteomyelitis and septic arthritis (SA) [1]. The development of these secondary infections as a consequence of their systemic infection [3]. The involvement of proinflammatory cytokines in the pathogenesis of S. aureus infection has been reported This bacteria can induce cytokines such as TNF-α, IFN-γ, IL-1, IL-2, and IL-6 [6,7]. Cytokines released from macrophages as TNF-α, IL-1β and IL-6 have been classically pointed as the major players of the severe inflammation that precedes cartilage and bone destruction in SA [2]. IL-17A appears to play a key role in host defense against local S. aureus infections by inducing the production of neutrophil-mobilizing chemokines, colony-stimulating factors, and cytokines [9]
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