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The brain is protected from penetrating pathogens by the blood-brain barrier and the innate immune system. The invading pathogens are recognized by pattern recognition receptors including the G-protein-coupled formyl peptide receptors (FPRs), which are expressed by immune cells of the central nervous system. FPRs show a broad spectrum of ligands, including pro- and anti-inflammatory ones. Here, we investigated the effects of the annexin A1 mimetic peptide Ac2-26 in a mouse model of pneumococcal meningitis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Wildtype (WT) and\n                      <jats:italic>Fpr1<\/jats:italic>\n                      - and\n                      <jats:italic>Fpr2<\/jats:italic>\n                      -deficient mice were intrathecally infected with\n                      <jats:italic>Streptococcus pneumoniae<\/jats:italic>\n                      D39 (type 2). Subsequently, the different mice groups were treated by intraperitoneal injections of Ac2-26 (1\u2009mg\/kg body weight) 2, 8, and 24\u2009h post-infection. The extent of inflammation was analyzed in various brain regions by means of immunohistochemistry and real-time reverse transcription polymerase chain reaction (RT-PCR) 30\u2009h post-infection.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Ac2-26-treated WT mice showed less severe neutrophil infiltration, paralleled by a reduced induction of pro-inflammatory glial cell responses in the hippocampal formation and cortex. While meningitis was ameliorated in Ac2-26-treated\n                      <jats:italic>Fpr1<\/jats:italic>\n                      -deficient mice, this protective effect was not observed in\n                      <jats:italic>Fpr2<\/jats:italic>\n                      -deficient mice. Irrespective of Ac2-26 treatment, inflammation was more severe in\n                      <jats:italic>Fpr2<\/jats:italic>\n                      -deficient compared to\n                      <jats:italic>Fpr1<\/jats:italic>\n                      -deficient mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      In summary, this study demonstrates anti-inflammatory properties of Ac2-26 in a model of bacterial meningitis, which are mediated via FPR2, but not FPR1. Ac2-26 and other FPR2 modulators might be promising targets for the development of novel therapies for\n                      <jats:italic>Streptococcus pneumoniae<\/jats:italic>\n                      -induced meningitis.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s12974-020-02006-w","type":"journal-article","created":{"date-parts":[[2020,10,29]],"date-time":"2020-10-29T14:03:12Z","timestamp":1603980192000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["The formyl peptide receptor agonist Ac2-26 alleviates neuroinflammation in a mouse model of pneumococcal meningitis"],"prefix":"10.1186","volume":"17","author":[{"given":"Marvin","family":"R\u00fcger","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eugenia","family":"Kipp","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nadine","family":"Schubert","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicole","family":"Schr\u00f6der","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"Pufe","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthias B.","family":"Stope","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Markus","family":"Kipp","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christian","family":"Blume","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Simone C.","family":"Tauber","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6126-8153","authenticated-orcid":false,"given":"Lars-Ove","family":"Brandenburg","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2020,10,29]]},"reference":[{"issue":"3","key":"2006_CR1","doi-asserted-by":"publisher","first-page":"557","DOI":"10.1128\/CMR.00008-11","volume":"24","author":"BB Mook-Kanamori","year":"2011","unstructured":"Mook-Kanamori BB, Geldhoff M, van der Poll T, van de Beek D. 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