{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,6,24]],"date-time":"2024-06-24T13:20:23Z","timestamp":1719235223117},"reference-count":49,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2015,9,6]],"date-time":"2015-09-06T00:00:00Z","timestamp":1441497600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100004663","name":"Ministry of Science and Technology, Taiwan","doi-asserted-by":"publisher","award":["103\u20102321\u2010B\u2010038\u2010002"],"award-info":[{"award-number":["103\u20102321\u2010B\u2010038\u2010002"]}],"id":[{"id":"10.13039\/501100004663","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Neuropathology Appl Neurobio"],"published-print":{"date-parts":[[2016,6]]},"abstract":"Aims<\/jats:title>Bacterial meningitis causes high mortality and brain damage. The host immune response is associated with brain injury. Chemokine (C<\/jats:styled-content>\u2010X<\/jats:styled-content>\u2010C<\/jats:styled-content> motif) (CXC<\/jats:styled-content>) chemokines are neutrophil chemoattractants. This study focused on the beneficial effects of intracerebroventricular administration of reparixin, an inhibitor of chemokine (C\u2010X\u2010C motif) receptor (CXCR<\/jats:styled-content>)1\/2, to rats at 2\u2009h following experimental K<\/jats:italic><\/jats:styled-content>lebsiella pneumoniae<\/jats:italic> meningoencephalitis.<\/jats:p><\/jats:sec>Methods<\/jats:title>We used a previously established meningoencephalitis animal model in which S<\/jats:styled-content>prague\u2010D<\/jats:styled-content>awley rats were infected by K<\/jats:italic><\/jats:styled-content>.\u2009pneumoniae<\/jats:italic>. Sham and infected animals were treated with vehicle or reparixin and sacrificed at various time points. Leukocyte infiltration into cerebrospinal fluid (CSF<\/jats:styled-content>) and brain as well as gene and protein expression of chemokines and receptors, and neuronal apoptosis were examined. Primary cultures of neuron\/glia were infected with K<\/jats:italic><\/jats:styled-content>.\u2009pneumoniae<\/jats:italic> as an in vitro<\/jats:italic> model of meningoencephalitis.<\/jats:p><\/jats:sec>Results<\/jats:title>Levels of chemokine (C\u2010X\u2010C motif) ligand (CXCL<\/jats:styled-content>)2 in CSF<\/jats:styled-content> time\u2010dependently increased markedly as early as 2\u2009h, and peaked at 8\u2009h following infection and were much higher than those in serum collected simultaneously. Reparixin significantly reduced leukocyte infiltration into CSF<\/jats:styled-content> and brain tissues, clinical illness, and brain cell apoptosis at 24\u2009h. Reparixin reduced the elevated CSF<\/jats:styled-content> concentrations of chemokines [CXCL<\/jats:styled-content>1, CXCL<\/jats:styled-content>2, chemokine (C<\/jats:styled-content>\u2010C<\/jats:styled-content> motif) ligand (CCL<\/jats:styled-content>)2 and CCL<\/jats:styled-content>5] and proinflammatory cytokines. Reparixin also reduced the expression of mRNA<\/jats:styled-content> of various chemokines, chemokine receptors and proinflammatory cytokines in infected brain tissues. Using primary cultures that are devoid of leukocytes, we further observed that reparixin attenuated the neuronal, but not microglial cell death after infection.<\/jats:p><\/jats:sec>Conclusions<\/jats:title>Reparixin not only reduces amplified inflammation, but also provides direct neuroprotective effects in K<\/jats:italic><\/jats:styled-content>.\u2009pneumoniae<\/jats:italic> meningoencephalitis.<\/jats:p><\/jats:sec>","DOI":"10.1111\/nan.12261","type":"journal-article","created":{"date-parts":[[2015,8,6]],"date-time":"2015-08-06T02:46:24Z","timestamp":1438829184000},"page":"326-343","source":"Crossref","is-referenced-by-count":2,"title":["Reparixin attenuates neuronal injury in experimental K<\/i><\/scp>lebsiella pneumoniae<\/i> meningoencephalitis through dual effects on neuroprotection and neuroinflammation"],"prefix":"10.1111","volume":"42","author":[{"given":"Chien\u2010Tsai","family":"Chiu","sequence":"first","affiliation":[{"name":"Department of Neurological Surgery 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