{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,7]],"date-time":"2026-04-07T17:02:36Z","timestamp":1775581356995,"version":"3.50.1"},"reference-count":67,"publisher":"American Society for Microbiology","issue":"8","license":[{"start":{"date-parts":[[2012,8,1]],"date-time":"2012-08-01T00:00:00Z","timestamp":1343779200000},"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":["Antimicrob Agents Chemother"],"published-print":{"date-parts":[[2012,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>Exacerbation of cerebrospinal fluid (CSF) inflammation in response to bacteriolysis by beta-lactam antibiotics contributes to brain damage and neurological sequelae in bacterial meningitis. Daptomycin, a nonlytic antibiotic acting on Gram-positive bacteria, lessens inflammation and brain injury compared to ceftriaxone. With a view to a clinical application for pediatric bacterial meningitis, we investigated the effect of combining daptomycin or rifampin with ceftriaxone in an infant rat pneumococcal meningitis model.<\/jats:p>\n          <jats:p>\n            <jats:bold>IMPORTANCE<\/jats:bold>\n            Eleven-day-old Wistar rats with pneumococcal meningitis were randomized to treatment starting at 18 h after infection with (i) ceftriaxone (100 mg\/kg of body weight, subcutaneously [s.c.], twice a day [b.i.d.]), (ii) daptomycin (10 mg\/kg, s.c., daily) followed 15 min later by ceftriaxone, or (iii) rifampin (20 mg\/kg, intraperitoneally [i.p.], b.i.d.) followed 15 min later by ceftriaxone. CSF was sampled at 6 and 22 h after the initiation of therapy and was assessed for concentrations of defined chemokines and cytokines. Brain damage was quantified by histomorphometry at 40 h after infection and hearing loss was assessed at 3 weeks after infection. Daptomycin plus ceftriaxone versus ceftriaxone significantly (\n            <jats:italic>P<\/jats:italic>\n            &lt; 0.04) lowered CSF concentrations of monocyte chemoattractant protein 1 (MCP-1), MIP-1\u03b1, and interleukin 6 (IL-6) at 6 h and MIP-1\u03b1, IL-6, and IL-10 at 22 h after initiation of therapy, led to significantly (\n            <jats:italic>P<\/jats:italic>\n            &lt; 0.01) less apoptosis, and significantly (\n            <jats:italic>P<\/jats:italic>\n            &lt; 0.01) improved hearing capacity. While rifampin plus ceftriaxone versus ceftriaxone also led to lower CSF inflammation (\n            <jats:italic>P<\/jats:italic>\n            &lt; 0.02 for IL-6 at 6 h), it had no significant effect on apoptosis and hearing capacity. Adjuvant daptomycin could therefore offer added benefits for the treatment of pediatric pneumococcal meningitis.\n          <\/jats:p>","DOI":"10.1128\/aac.00674-12","type":"journal-article","created":{"date-parts":[[2012,5,30]],"date-time":"2012-05-30T03:24:37Z","timestamp":1338348277000},"page":"4289-4295","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":37,"title":["Adjunctive Daptomycin Attenuates Brain Damage and Hearing Loss More Efficiently than Rifampin in Infant Rat Pneumococcal Meningitis"],"prefix":"10.1128","volume":"56","author":[{"given":"Denis","family":"Grandgirard","sequence":"first","affiliation":[{"name":"Neuroinfection Laboratory, Institute for Infectious Diseases, University of Bern, Switzerland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Melchior","family":"Burri","sequence":"additional","affiliation":[{"name":"Neuroinfection Laboratory, Institute for Infectious Diseases, University of Bern, Switzerland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Philipp","family":"Agyeman","sequence":"additional","affiliation":[{"name":"Neuroinfection Laboratory, Institute for Infectious Diseases, University of Bern, Switzerland"},{"name":"Department of Pediatric Infectiology, Inselspital, University Hospital, Bern, Switzerland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stephen L.","family":"Leib","sequence":"additional","affiliation":[{"name":"Neuroinfection Laboratory, Institute for Infectious Diseases, University of Bern, Switzerland"},{"name":"Biology Division, Spiez Laboratory, Federal Office for Civil Protection, Spiez, Switzerland"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1462-5822.2005.00578.x"},{"key":"e_1_3_2_3_2","doi-asserted-by":"crossref","first-page":"1154","DOI":"10.1097\/00005344-198511000-00022","article-title":"Myeloperoxidase activity as a quantitative marker of polymorphonuclear leukocyte accumulation into an experimental myocardial infarct\u2014the effect of ibuprofen on infarct size and polymorphonuclear leukocyte accumulation","volume":"7","author":"Allan G","year":"1985","unstructured":"AllanG BhattacherjeeP BrookCD ReadNG ParkeAJ. 1985. 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