{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T03:24:53Z","timestamp":1790911493553,"version":"4.1.0"},"reference-count":32,"publisher":"American Society for Microbiology","issue":"9","license":[{"start":{"date-parts":[[2010,9,1]],"date-time":"2010-09-01T00:00:00Z","timestamp":1283299200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2010,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p><jats:italic>Staphylococcus aureus<\/jats:italic>is one of the dominant pathogens that induce septic arthritis in immunocompromised hosts, e.g., patients suffering from rheumatoid arthritis treated with immunosuppressive drugs.<jats:italic>S. aureus<\/jats:italic>-induced arthritis leads to severe joint destruction and high mortality despite antibiotic treatment. Recently, interleukin-17A (IL-17A) has been discovered to be an important mediator of aseptic arthritis both in mice and humans, but its function in<jats:italic>S. aureus<\/jats:italic>-induced arthritis is largely unknown. Here, we investigated the role of IL-17A in host defense against arthritis following systemic and local<jats:italic>S. aureus<\/jats:italic>infection<jats:italic>in vivo<\/jats:italic>. IL-17A knockout mice and wild-type mice were inoculated systemically (intravenously) or locally (intra-articularly) with<jats:italic>S. aureus<\/jats:italic>. During systemic infection, IL-17A knockout mice lost significantly more weight than the wild-type mice did, but no differences were found in the mortality rate. The absence of IL-17A had no impact on clinical arthritis development but led to increased histopathological erosivity late during systemic<jats:italic>S. aureus<\/jats:italic>infection. Bacterial clearance in kidneys was increased in IL-17A knockout mice compared to the level in wild-type mice only 1 day after bacterial inoculation. During systemic<jats:italic>S. aureus<\/jats:italic>infection, serum IL-17F protein levels and mRNA levels in the lymph nodes were elevated in the IL-17A knockout mice compared to the level in wild-type mice. In contrast to systemic infection, the IL-17A knockout mice had increased synovitis and erosions and locally decreased clearance of bacteria 3 days after local bacterial inoculation. On the basis of these findings, we suggest that IL-17A is more important in local host defense than in systemic host defense against<jats:italic>S. aureus<\/jats:italic>-induced arthritis.<\/jats:p>","DOI":"10.1128\/iai.00385-10","type":"journal-article","created":{"date-parts":[[2010,6,29]],"date-time":"2010-06-29T04:19:20Z","timestamp":1277785160000},"page":"3783-3790","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":29,"title":["Interleukin-17A during Local and Systemic<i>Staphylococcus aureus<\/i>-Induced Arthritis in Mice"],"prefix":"10.1128","volume":"78","author":[{"given":"Louise","family":"Henningsson","sequence":"first","affiliation":[{"name":"Department of Rheumatology and Inflammation Research"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pernilla","family":"Jirholt","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Inflammation Research"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Catharina","family":"Lindholm","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Inflammation Research"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tove","family":"Eneljung","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Inflammation Research"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elin","family":"Silverpil","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine\/Respiratory Medicine and Allergology, Institute of Medicine, University of Gothenburg, Gothenburg, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoichiro","family":"Iwakura","sequence":"additional","affiliation":[{"name":"Center for Experimental Medicine and Systems Biology, Institute of Medical Science, University of Tokyo, and Core Research for Evolutional Science and Technology (CREST), Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anders","family":"Linden","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine\/Respiratory Medicine and Allergology, Institute of Medicine, University of Gothenburg, Gothenburg, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Inger","family":"Gjertsson","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Inflammation Research"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.60.7.2976-2985.1992"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1002\/art.1780331120"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1002\/1529-0131(199905)42:5<963::AID-ANR15>3.0.CO;2-E"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajplung.00312.2006"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cyto.2008.07.017"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1002\/art.27334"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20050193"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1038\/ni1254"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.177.11.7980"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.165.11.6107"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2008.11.009"},{"key":"e_1_3_2_13_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.00724-09"},{"key":"e_1_3_2_14_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.tips.2008.11.004"},{"key":"e_1_3_2_15_2","unstructured":"Reference deleted."},{"key":"e_1_3_2_16_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2004.08.018"},{"key":"e_1_3_2_17_2","doi-asserted-by":"crossref","first-page":"2347","DOI":"10.4049\/jimmunol.162.4.2347","volume":"162","year":"1999","unstructured":"Laan, M., Z. 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