{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T06:26:40Z","timestamp":1788848800485,"version":"build-2803163510"},"reference-count":38,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2005,2,18]],"date-time":"2005-02-18T00:00:00Z","timestamp":1108684800000},"content-version":"vor","delay-in-days":2120,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal Orthopaedic Research"],"published-print":{"date-parts":[[1999,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>A murine model of acute hematogenous osteomyelitis was used to study the immune response following <jats:italic>Staphylococcus aureus<\/jats:italic> infection and to examine the hypothesis that the bacteria may modify T\u2010cell responses due to the production of bacterial enterotoxins with mitogenic or superantigenic activity. Lymphnode T cell\u2010receptor expression was assessed with use of flow cytometry and reverse transcription\u2010polymerase chain reaction techniques, and increased apoptosis (programmed cell death) in T\u2010cell subsets was monitored. The expression and levels of circulating cytokines and T\u2010cell cytokines within tissues surrounding the damaged area of the proximal tibia were also investigated. Analysis of T\u2010cell receptors in experimental osteomyelitis revealed two distinct patterns of T\u2010cell evolution during the disease. Certain T\u2010cell subsets (V\u03b22, V\u03b23, V\u03b29, and V\u03b210) were activated and expanded during the first 24 hours after infection; they reached maximum levels 6 days after infection, followed by a return to pre\u2010infection levels. In contrast, other T\u2010cell subsets (V\u03b211, V\u03b212, V\u03b213, V\u03b214, and V\u03b216) contracted during the first 24 hours after infection, followed by expansion to a maximum level 9 days after infection. Activation and proliferation of T\u2010cell subsets (notably V\u03b214 T cells) was followed by apoptosis, suggesting that staphylococcal bone infection caused superantigenic\u2010like effects on the mouse immune system. Analysis of cytokine responses in local tissue revealed that the T\u2010cell cytokines interleukin\u20102 and interferon\u2010\u03b3 showed a late and relatively short activation pattern compared with the inflammatory cytokines interleukin\u20101, interleukin\u20106, and tumor necrosis factor\u2010\u03b1. The results suggest that <jats:italic>Staphylococcus aureus<\/jats:italic> bone infection may undermine the antibacterial immune response through downregulation of T\u2010cell immunity and immune\u2010cytokine production, which could increase the severity of the systemic infection and local osseous destruction that occur with acute hematogenous osteomyelitis.<\/jats:p>","DOI":"10.1002\/jor.1100170313","type":"journal-article","created":{"date-parts":[[2005,2,24]],"date-time":"2005-02-24T10:25:00Z","timestamp":1109240700000},"page":"382-391","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":33,"title":["Experimental acute hematogenous osteomyelitis in mice. II. Influence of <i>Staphylococcus aureus<\/i> infection on T\u2010cell immunity"],"prefix":"10.1002","volume":"17","author":[{"given":"K. S.","family":"Yoon","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"Jr.","given":"R. 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