Wellmer, Andreas

[["dc.bibliographiccitation.firstpage","6881"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Infection and Immunity"],["dc.bibliographiccitation.lastpage","6886"],["dc.bibliographiccitation.volume","69"],["dc.contributor.author","Wellmer, A."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Ragheb, J."],["dc.contributor.author","Zysk, G."],["dc.contributor.author","Kunst, T."],["dc.contributor.author","Smirnov, Alexey"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T08:28:39Z"],["dc.date.available","2018-11-07T08:28:39Z"],["dc.date.issued","2001"],["dc.description.abstract","Tumor necrosis factor alpha (TNF-alpha) and TNF-beta are key mediators in bacterial inflammation. We therefore examined the role of TNF-alpha and its two receptors in murine pneumococcal central nervous system infection. TNF-alpha knockout mice and age- and sex-matched controls and TNF receptor (p55 and p75)-deficient mice and heterozygous littermates were infected intracerebrally with a Streptococcus pneumoniae type 3 strain. Mice were monitored until death or were killed 36 h after infection. Bacterial titers in blood, spleen, and brain homogenates were determined. Leukocyte infiltration and neuronal damage were assessed by histological scores. TNF-alpha -deficient mice died earlier than the controls after intracerebral infection although overall survival was similar. TNF-alpha deficiency did not inhibit leukocyte, recruitment into the subarachnoid space and did not lead to an increased density of bacteria in brain homogenates. However, it caused a substantial rise of the concentration of S. pneumoniae cells in blood and spleen. Spleen bacterial titers were also increased in p55- and p75-deficient mice. TNF receptor-deficient mice showed decreased meningeal inflammation. Neuronal damage was not affected by either TNF-alpha or TNT receptor deficiency. In a murine model of pneumococcal peritonitis, 10(2) CFU of S. pneumoniae produced fatal peritonitis in TNF-alpha -deficient, but not wild-type, mice. Early leukocyte influx into the peritoneum was impaired in TNF-alpha -deficient mice. The lack of TNF-alpha or its receptors renders mice more susceptible to S. pneumoniae infections."],["dc.identifier.doi","10.1128/IAI.69.11.6881-6886.2001"],["dc.identifier.isi","000171739200040"],["dc.identifier.pmid","11598062"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16471"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Microbiology"],["dc.relation.issn","0019-9567"],["dc.title","Effect of deficiency of tumor necrosis factor alpha or both of its receptors on Streptococcus pneumoniae central nervous system infection and peritonitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","175"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","European Journal of Paediatric Neurology"],["dc.bibliographiccitation.lastpage","178"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Wellmer, Andreas"],["dc.contributor.author","Rostasy, Kevin"],["dc.contributor.author","Baehr, Mathias"],["dc.contributor.author","Kermer, Pawel"],["dc.date.accessioned","2017-09-07T11:48:57Z"],["dc.date.available","2017-09-07T11:48:57Z"],["dc.date.issued","2012"],["dc.description.abstract","NBIA/HSS is a neurodegenerative disorder associated with iron accumulation in specific brain regions. To date, the diagnosis is obtained by typical MRI changes followed by genetic mutation analysis. This procedure is laborious and limited to a few specially equipped medical centres. Since transcranial sonography (TCS) is widely used for the early diagnosis of PD in adults displaying parenchymal metal deposits, it is likely to be a reliable diagnostic tool for the early diagnosis of NBIA. In 7 patients with proven NBIA and 13 age-matched controls without record of neurological disease TCS was performed by an experienced ultrasound examiner. Data were analysed by two blinded investigators regarding hyperechogenicity and size of the substantia nigra (SN). SN size and hyperechogenicity was significantly increased in patients with NBIA compared to controls (students t-test: p < 0.001). TCS appears to be a non-invasive and inexpensive screening technique in patients with suspected NBIA. Performed by an experienced physician, it could enable an earlier diagnosis and pre-selection of patients for the MRI scan and genetic testing, which are still the diagnostic gold standard. (C) 2011 European Paediatric Neurology Society. Published by Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.ejpn.2011.07.009"],["dc.identifier.gro","3142571"],["dc.identifier.isi","000301216700011"],["dc.identifier.pmid","21816641"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8936"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1090-3798"],["dc.title","Transcranial ultrasound in neurodegeneration with brain iron accumulation (NBIA)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3113"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Infection and Immunity"],["dc.bibliographiccitation.lastpage","3119"],["dc.bibliographiccitation.volume","72"],["dc.contributor.author","Wellmer, A."],["dc.contributor.author","von Mering, M."],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Diem, Ricarda"],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Noeske, C."],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T10:48:28Z"],["dc.date.available","2018-11-07T10:48:28Z"],["dc.date.issued","2004"],["dc.description.abstract","Necrotic and apoptotic neuronal cell death can be found in pneumococcal meningitis. We investigated the role of Bcl-2 as an antiapoptotic gene product in pneumococcal meningitis using Bcl-2 knockout (Bcl-2(-/-)) mice. By using a model of pneumococcal meningitis induced by intracerebral infection, Bcl-2-deficient mice and control littermates were assessed by clinical score and a tight rope test at 0, 12, 24, 32, and 36 h after infection. Then mice were sacrificed, the bacterial titers in blood, spleen, and cerebellar homogenates were determined, and the brain and spleen were evaluated histologically. The Bcl-2-deficient mice developed. more severe clinical illness, and there were significant differences in the clinical score at 24, 32, and 36 h and in the tight rope test at 12 and 32 h. The bacterial titers in the blood were greater in Bcl-2-deficient mice than in the controls (7.46 +/- 1.93 log CFU/ml versus 5.16 +/- 0.96 log CFU/ml [mean +/- standard deviation]; P < 0.01). Neuronal damage was most prominent in the hippocampal formation, but there were no significant differences between groups. In situ tailing revealed only a few apoptotic neurons in the brain. In the spleen, however, there were significantly more apoptotic leukocytes in Bcl-2-deficient mice than in controls (5,148 +/- 3,406 leakocytes/mm(2) versus 1,070 +/- 395 leukocytes/mm(2); p < 0.005). Bcl-2 appears to counteract sepsis-induced apoptosis of splenic lymphocytes, thereby enhancing clearance of bacteria from the blood."],["dc.identifier.doi","10.1128/IAI.72.6.3113-3119.2004"],["dc.identifier.isi","000221662400004"],["dc.identifier.pmid","15155612"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48200"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Microbiology"],["dc.relation.issn","0019-9567"],["dc.title","Experimental pneumococcal meningitis: Impaired clearance of bacteria from the blood due to increased apoptosis in the spleen in Bcl-2-deficient mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","909"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Scandinavian Journal of Infectious Diseases"],["dc.bibliographiccitation.lastpage","913"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Wellmer, A."],["dc.contributor.author","Prange, J."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Zysk, G."],["dc.contributor.author","Lange, P."],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T09:39:30Z"],["dc.date.available","2018-11-07T09:39:30Z"],["dc.date.issued","2001"],["dc.description.abstract","Increased total CSF lactate is an important indicator differentiating bacterial from aseptic meningitis. Bacteria can produce D- and L-lactate; mammalian cells produce only L-lactate. We measured D- and L-lactate production of Streptococcus pneumoniae, Staphylococcus aureus, Neisseria meningitidis and Escherichia coli in vitro, of S. pneumoniae and E. coli in rabbit experimental meningitis and of various common pathogens in CSF from patients with bacterial meningitis. Despite marked in vitro production of D-lactate by S. aureus (maximum: 4.59 mmol/l; i.e. 34.9% of total lactate), N. meningitidis (4.62 mmol/l; i.e. 98.1%) and E. coli (3.14 mmol/l; i.e. 97.2%), minimal amounts were measured in human S. aureus (0.38 mmol/l; i.e. 1.3% of total lactate) or N. meningitidis (0.28 mmol/l; i.e. 3.9%) and experimental E. coli meningitis (0.75 mmol/l; i.e. 4.4%). In only 9 of 54 human CSF samples did D-lactate exceed 0.15 mmol/l. S. pneumoniae did not produce significant amounts of D-lactate in vitro (maximum; 0.55 mmol/l; i.e. 2.7% of total lactate), in experimental meningitis (0.18 mmol/l; i.e. 3%) or in human cases of meningitis (0.28 mmol/l; i.e. 1.9%). In conclusion, increased total CSF lactate in meningitis consists mainly of L-lactate and originates predominantly from host cells. CSF D-lactate is of limited diagnostic value."],["dc.identifier.isi","000173355800006"],["dc.identifier.pmid","11868764"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33300"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Taylor & Francis As"],["dc.publisher.place","Oslo"],["dc.relation.conference","40th Interscience Conference on Antimicrobial Agents and Chemotherapy"],["dc.relation.eventlocation","TORONTO, CANADA"],["dc.relation.issn","0036-5548"],["dc.title","D- and L-lactate in rabbit and human bacterial meningitis"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","325"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neurocritical Care"],["dc.bibliographiccitation.lastpage","329"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Djukic, M."],["dc.contributor.author","Bottcher, T."],["dc.contributor.author","Wellmer, A."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Brocke, V. V."],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T08:44:15Z"],["dc.date.available","2018-11-07T08:44:15Z"],["dc.date.issued","2005"],["dc.description.abstract","Rifampin, a protein synthesis inhibitor, reduced mortality in a mouse model of meningitis compared to bacteriolytic cephalosporin standard therapy. To assess whether moxifloxacin (known to cause a less rapid bacteriolysis than cephalosporins) can similarly reduce mortality, mice infected with Streptococcus pneumoniae by deep intracerebral injection were treated subcutaneously with either 200 mg/kg of moxifloxacin or ceftriaxone every 8 hours for 5 days (n=49 each). They were then observed for an additional 8 days. Overall mortalities were 35 and 29 in moxifloxacin- and ceftriaxone-treated mice, respectively (p=0.29). Kaplan-Meier survival analysis also revealed no statistically significant differences (p=0.32). Moxifloxacin failed to reduce mortality compared to cephalosporin standard therapy."],["dc.identifier.doi","10.1385/NCC:2:3:325"],["dc.identifier.isi","000231204500015"],["dc.identifier.pmid","16159084"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20158"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Humana Press Inc"],["dc.relation.issn","1541-6933"],["dc.title","Moxifloxacin in experimental Streptococcus pneumoniae cerebritis and meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","137"],["dc.bibliographiccitation.issue","2-3"],["dc.bibliographiccitation.journal","Neuroscience Letters"],["dc.bibliographiccitation.lastpage","140"],["dc.bibliographiccitation.volume","296"],["dc.contributor.author","Wellmer, A."],["dc.contributor.author","Noeske, C."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Munzel, U."],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T11:20:54Z"],["dc.date.available","2018-11-07T11:20:54Z"],["dc.date.issued","2000"],["dc.description.abstract","Survivors of bacterial meningitis frequently suffer from long-term sequelae, particularly from learning and memory deficits. For this reason, spatial memory and learning was studied in a mouse model of ceftriaxone-treated Streptococcus pneumoniae meningitis. Persistent deficits of spatial learning despite normal motor function were observed in mice infected with 10(4) colony-forming units (CFU) in 25 mul of saline into the right forebrain in comparison to mice treated with an equal amount of saline. Survivors of meningitis performed significantly worse in memorizing a hidden platform in a Morris water maze. After 2 weeks, the difference between post-meningitis and control mice diminished. Yet, when the platform was moved after 180 days, learning of the new location was still strongly impaired in mice surviving meningitis. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/S0304-3940(00)01645-1"],["dc.identifier.isi","000165859800019"],["dc.identifier.pmid","11109000"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55647"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Sci Ireland Ltd"],["dc.relation.issn","0304-3940"],["dc.title","Spatial memory and learning deficits after experimental pneumococcal meningitis in mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","767"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Antimicrobial Agents and Chemotherapy"],["dc.bibliographiccitation.lastpage","770"],["dc.bibliographiccitation.volume","44"],["dc.contributor.author","Smirnov, Alexey"],["dc.contributor.author","Wellmer, A."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Maier, K."],["dc.contributor.author","Henne, S."],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T08:56:14Z"],["dc.date.available","2018-11-07T08:56:14Z"],["dc.date.issued","2000"],["dc.description.abstract","In a rabbit model of Streptococcus pneumoniae meningitis, 5 mg of gemifloxacin mesylate (SB-265805) per kg/h reduced the bacterial titers in cerebrospinal fluid (CSF) almost as rapidly as 10 mg of ceftriaxone per kg/h (Delta log CFU/ml/h +/- standard deviation [SD], -0.25 +/- 0.09 versus -0.38 +/- 0.11; serum and CSF concentrations of gemifloxacin were 2.1 +/- 1.4 mg/liter and 0.59 +/- 0.38 mg/liter, respectively, at 24 h). Coadministration of 1 mg of dexamethasone per kg did not affect gemifloxacin serum and CSF levels (2.7 +/- 1.4 mg/liter and 0.75 +/- 0.34 mg/liter, respectively, at 24 h) or activity (Delta log CFU/ml/h +/- SD, -0.26 +/- 0.11)."],["dc.identifier.doi","10.1128/AAC.44.3.767-770.2000"],["dc.identifier.isi","000085399200049"],["dc.identifier.pmid","10681354"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23091"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Microbiology"],["dc.relation.issn","0066-4804"],["dc.title","Gemifloxacin is effective in experimental pneumococcal meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","282"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Brain Pathology"],["dc.bibliographiccitation.lastpage","295"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Mering, Matthias"],["dc.contributor.author","Wellmer, Andreas"],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Tłustochowska, Anna"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Kuhnt, Ulrich"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2021-06-01T10:47:22Z"],["dc.date.available","2021-06-01T10:47:22Z"],["dc.date.issued","2001"],["dc.description.abstract","Apoptosis and necrosis in brain account for neurological sequelae in survivors of bacterial meningitis. In meningitis, several mechanisms may trigger death pathways leading to activation of transcription factors regulating caspases mRNA synthesis. Therefore, we used a multiprobe RNA protection assay (RPA) to examine the expression of 9 caspase-6-mRNA in the course of experimental Streptococcus pneumoniae meningitis in mouse brain. Caspase-6, -7 and -11 mRNA were elevated 6 hours after infection. 12 hours after infection caspases-1, -2, -8 and 12 mRNA rose. Caspase-14 mRNA was elevated 18 h and caspase-3 mRNA 24 h after infection. In situ hybridization detected caspases-3, -8, -11 and -12 mRNA in neurons of the hippocampal formation and neocortex. Development of sepsis was paralleled by increased transcription of caspases mRNA in the spleen. In TNF alpha -deficient mice all caspases examined were less upregulated, in TNF-receptor 1/2 knockout mice caspases-1, -2, -7, -11 and -14 mRNA were increased compared to infected control animals. In caspase-1 deficient mice, caspases-11, and -12 mRNA levels did not rise in meningitis indicating the necessity of caspase-1 activating these caspases. Hippocampal formations of newborn mice incubated with heat-inactivated S. pneumoniae R6 showed upregulation of caspase-1, -3, -11 and -12 mRNA. These observations suggest a tightly regulated caspases network at the transcriptional level in addition to the known cascade at the protein level."],["dc.identifier.doi","10.1111/j.1750-3639.2001.tb00399.x"],["dc.identifier.isi","000168965400002"],["dc.identifier.pmid","11414471"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85576"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Int Soc Neuropathology"],["dc.relation.issn","1015-6305"],["dc.title","Transcriptional Regulation of Caspases in Experimental Pneumococcal Meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","315"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Ultrasound in Medicine & Biology"],["dc.bibliographiccitation.lastpage","320"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Kermer, Pawel"],["dc.contributor.author","Wellmer, Andreas"],["dc.contributor.author","Crome, Olaf"],["dc.contributor.author","Mohr, Alexander"],["dc.contributor.author","Knauth, Michael"],["dc.contributor.author","Bähr, Mathias"],["dc.date.accessioned","2017-09-07T11:53:17Z"],["dc.date.available","2017-09-07T11:53:17Z"],["dc.date.issued","2006"],["dc.description.abstract","Transcranial color-coded duplex sonography (TCDS) is a noninvasive, quick and inexpensive diagnostic tool used routinely to assess vascular abnormalities in cerebral ischemia. The value of TCDS for diagnosis and follow-up of acute basilar artery (BA) ischemia in comparison/combination with spiral CT angiography (CTA) and/or digital subtraction angiography (DSA) has not vet been studied. We prospectively studied 15 consecutive patients with clinically suspected acute BA occlusion (BAO) by TCDS as well as 3 to 5 d later in those with proven BAO. BA ischemia was verified in 11 patients. During follow-up, all BAO patients showed recanalization of the BA independent of thrombolytic treatment. In conclusion, TCDS appears to be an efficient method for BAO diagnosis when immediate angiography is not available. Together with CTA it increases diagnostic safety before performing an invasive and cost-intensive DSA. (C) 2006 World Federation for Ultrasound in Medicine & Biology."],["dc.identifier.doi","10.1016/j.ultrasmedbio.2005.12.004"],["dc.identifier.gro","3143733"],["dc.identifier.isi","000236260100002"],["dc.identifier.pmid","16530089"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1280"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0301-5629"],["dc.title","Transcranial color-coded duplex sonography in suspected acute basilar artery occlusion"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1560"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Critical Care Medicine"],["dc.bibliographiccitation.lastpage","1564"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Azeh, I."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Wellmer, A."],["dc.contributor.author","Wellhausen, M."],["dc.contributor.author","Koenig, B."],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T10:20:11Z"],["dc.date.available","2018-11-07T10:20:11Z"],["dc.date.issued","2002"],["dc.description.abstract","Objective: The release of proinflammatory components from bacteria depends on the mode of action of the antibacterial therapy used. We studied whether this influences mortality in experimental sepsis. Design. In a lethal murine model of Staphylococcus aureus sepsis, animals were randomly assigned to receive the protein synthesis inhibitor clindamycin (CLI) or the beta-lactam ceftriaxone (CRO). Setting. Therapy was introduced subcutaneously 5 hrs after intraperitoneal injection of 107 colony forming units of S. aureus American Type Culture Collection 29213 and was continued every 8 hrs for 3 days. Measurements and Results: Survival was higher in mice receiving CLI (29/50 animals [58%]) than in mice receiving CRO (16/50 animals [32%]; p = 015). Mice treated with CRO died earlier than mice receiving CLI (p = .002). Eight hours after the first antibiotic dose, the motor performance of mice receiving CRO had deteriorated more than it did for mice receiving CLI (p = .009). Higher levels of tumor necrosis factor-alpha were measured in serum (p = .027) and peritoneal fluid (p = .001) of CRO-treated mice. In vitro, CLI released smaller amounts of staphylococcal enterotoxin A than CRO. Conclusions: Antibiotic treatment of Gram-positive sepsis with a protein synthesis inhibitor decreases morbidity and mortality compared with a bacteriolytic compound. This may be caused by a reduction of the concentrations of proinflammatory/toxic bacterial components and cytokines."],["dc.identifier.doi","10.1097/00003246-200207000-00027"],["dc.identifier.isi","000176841100027"],["dc.identifier.pmid","12130979"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41828"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0090-3493"],["dc.title","Protein synthesis inhibiting clindamycin improves outcome in a mouse model of Staphylococcus aureus sepsis compared with the cell wall active ceftriaxone"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]