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Inflammation triggered in response to infection is fundamental to control bacterial growth but may cause permanent tissue damage. Here, we evaluated the role of Lipoxin A\n                    <jats:sub>4<\/jats:sub>\n                    (LXA\n                    <jats:sub>4<\/jats:sub>\n                    ) in\n                    <jats:italic>S aureus\u2010<\/jats:italic>\n                    induced arthritis in mice. Septic arthritis was induced by\n                    <jats:italic>S aureus<\/jats:italic>\n                    injection into tibiofemoral joints. At different time points, we evaluated cell recruitment and bacterial load in the joint, the production of pro\u2010inflammatory molecules, and LXA\n                    <jats:sub>4<\/jats:sub>\n                    in inflamed tissue and analyzed joint damage and dysfunction. LXA\n                    <jats:sub>4<\/jats:sub>\n                    was investigated using genetically modified mice or by pharmacological blockade of its synthesis and receptor. CD11c\n                    <jats:sup>+<\/jats:sup>\n                    cells were evaluated in lymph nodes by confocal microscopy and flow cytometry and dendritic cell chemotaxis using the Boyden chamber. Absence or pharmacological blockade of 5\u2010lipoxygenase (5\u2010LO) reduced joint inflammation and dysfunction and was associated with better control of\u00a0infection at 4 to 7\u00a0days after the infection. There was an increase in LXA\n                    <jats:sub>4<\/jats:sub>\n                    in joints of\u00a0\n                    <jats:italic>S aureus<\/jats:italic>\n                    \u2010infected mice and administration of LXA\n                    <jats:sub>4<\/jats:sub>\n                    reversed the phenotype in 5\u2010LO\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice. Blockade or absence of the LXA\n                    <jats:sub>4<\/jats:sub>\n                    receptor FPR2 has a phenotype similar to 5\u2010LO\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice. Mechanistically, LXA\n                    <jats:sub>4<\/jats:sub>\n                    appeared to control migration and function of dendritic cells, cells shown to be crucial for adequate protective responses in the model. Thus, after the first days of infection when symptoms become evident therapies that inhibit LXA\n                    <jats:sub>4<\/jats:sub>\n                    synthesis or action could be useful for treatment of\n                    <jats:italic>S aureus<\/jats:italic>\n                    \u2010induced arthritis.\n                  <\/jats:p>","DOI":"10.1096\/fj.201802830rr","type":"journal-article","created":{"date-parts":[[2020,8,2]],"date-time":"2020-08-02T05:20:30Z","timestamp":1596345630000},"page":"11498-11510","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Lipoxin A\n                    <sub>4<\/sub>\n                    impairs effective bacterial control and potentiates joint inflammation and damage caused by\n                    <i>Staphylococcus aureus<\/i>\n                    infection"],"prefix":"10.1096","volume":"34","author":[{"given":"Daiane","family":"Boff","sequence":"first","affiliation":[{"name":"Immunopharmacology Department of Biochemistry and Immunology Instituto de Ci\u00eancias Biol\u00f3gicas Universidade Federal de Minas Gerais Belo Horizonte Brazil"},{"name":"Laboratory of Molecular Immunology Department of Microbiology and Immunology Rega Institute for Medical Research KU Leuven Leuven Belgium"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Vivian Louise Soares","family":"Oliveira","sequence":"additional","affiliation":[{"name":"Immunopharmacology Department of Biochemistry and Immunology Instituto de Ci\u00eancias Biol\u00f3gicas Universidade Federal de Minas Gerais Belo Horizonte Brazil"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Celso M.","family":"Queiroz Junior","sequence":"additional","affiliation":[{"name":"Department of Morphology Instituto de Ci\u00eancias Biol\u00f3gicas Universidade Federal 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