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Superantigens produced by <jats:italic>S. aureus<\/jats:italic> are considered the major arthritogenic factors. In this study, we compared the arthritogenic potential of five superantigen-producing staphylococcal strains.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods<\/jats:title>\n            <jats:p>Male C57BL\/6 mice were intravenously infected with ATCC 19095 SEC<jats:sup>+<\/jats:sup>, N315 ST5 TSST-1<jats:sup>+<\/jats:sup>, S-70 TSST-1<jats:sup>+<\/jats:sup>, ATCC 51650 TSST-1<jats:sup>+<\/jats:sup> and ATCC 13565 SEA<jats:sup>+<\/jats:sup> 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.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>Weight loss was observed in all infected mice. ATCC 19095 SEC<jats:sup>+<\/jats:sup>, N315 ST5 TSST-1<jats:sup>+<\/jats:sup> and S-70 TSST-1<jats:sup>+<\/jats:sup> were arthritogenic, being the highest scores observed in ATCC 19095 SEC<jats:sup>+<\/jats:sup> infected mice. Intermediate and lower clinical scores were observed in N315 ST5 TSST-1<jats:sup>+<\/jats:sup> and S-70 TSST-1<jats:sup>+<\/jats:sup> infected mice, respectively. The ATCC 13565 SEA<jats:sup>+<\/jats:sup> strain caused death of 85% of the animals after 48\u00a0h. Arthritis triggered by the ATCC 19095 SEC<jats:sup>+<\/jats:sup> 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<jats:sup>+<\/jats:sup> infected mice, however they were strikingly more discrete. Only minor synovial proliferation and inflammation were triggered by the S-70 TSST-1<jats:sup>+<\/jats:sup> strain. The lowest levels of TNF-\u03b1, IL-6 and IL-17 production in response to <jats:italic>S. aureus<\/jats:italic> stimulation were found in cultures from mice infected with the less arthritogenic strains (S-70 TSST-1<jats:sup>+<\/jats:sup> and ATCC 51650 TSST-1<jats:sup>+<\/jats:sup>). The highest production of IL-17 was detected in mice infected with the most arthritogenic strains (ATCC 19095 SEC<jats:sup>+<\/jats:sup> and N315 ST5 TSST-1<jats:sup>+<\/jats:sup>).<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p>Together these results demonstrated that <jats:italic>S. aureus<\/jats:italic> 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.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/1471-2334-13-400","type":"journal-article","created":{"date-parts":[[2013,8,30]],"date-time":"2013-08-30T02:19:55Z","timestamp":1377829195000},"update-policy":"http:\/\/dx.doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Differential arthritogenicity of Staphylococcus aureusstrains isolated from biological samples"],"prefix":"10.1186","volume":"13","author":[{"given":"Priscila Maria","family":"Colavite-Machado","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Larissa Lumi Watanabe","family":"Ishikawa","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tha\u00eds Graziela","family":"Doneg\u00e1 Fran\u00e7a","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sofia Fernanda Gon\u00e7alves","family":"Zorzella-Pezavento","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Larissa Camargo","family":"da Rosa","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Fernanda","family":"Chiuso-Minicucci","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Maria de Lourdes Ribeiro de Souza","family":"da Cunha","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gustavo Pompermaier","family":"Garlet","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alexandrina","family":"Sartori","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2013,8,30]]},"reference":[{"key":"2647_CR1","doi-asserted-by":"publisher","first-page":"184","DOI":"10.1016\/j.tim.2010.12.005","volume":"4","author":"AM Edwards","year":"2011","unstructured":"Edwards AM, Massey RC: How does Staphylococcus aureus escape the bloodstream?. 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