Spreer, Annette

[["dc.bibliographiccitation.firstpage","210"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Pediatric Research"],["dc.bibliographiccitation.lastpage","215"],["dc.bibliographiccitation.volume","60"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Hanssen, Mareike"],["dc.contributor.author","Schindler, Stefanie"],["dc.contributor.author","Hermann, Corinna"],["dc.contributor.author","Lange, Peter"],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2018-11-07T09:30:34Z"],["dc.date.available","2018-11-07T09:30:34Z"],["dc.date.issued","2006"],["dc.description.abstract","Mortality and long-term sequelae rates are high among adults and children with acute bacterial meningitis. Adjunctive treatment with dexamethasone has been shown to reduce systemic complications in bacteria] meningitis patients, but corticosteroid treatment may have detrimental effects on hippocampal function. We evaluated the effect of dexamethasone treatment in addition to antibiotic therapy in a rabbit model of Escherichia coli meningitis. A moderate anti-inflammatory effect of dexamethasone could be demonstrated with respect to the inflammatory mediator prostaglandin E2, whereas no significant effect of dexamethasone on tumor necrosis factor-alpha, cerebrospinal fluid pleocytosis, protein, lactate, indicators of global neuronal damage, or blood gas analysis was found. Dexamethasone, however, increased the rate of apoptotic neurons in the granular layer of the hippocampal dentate gyrus. In view of the proapoptotic effect of adjunctive dexamethasone on hippocampal neuronal cells in animal models of Gram-positive and Gram-negative meningitis, the application of dexamethasone should be considered carefully in those forms of bacterial meningitis for which no evidence-based data of beneficial effect in humans are available, such as neonatal meningitis, bacillary Gram-negative meningitis or nosocomial forms of meningitis (e.g. following neurosurgery)."],["dc.identifier.doi","10.1203/01.pdr.0000227553.47378.9f"],["dc.identifier.isi","000239195300019"],["dc.identifier.pmid","16864706"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31335"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Int Pediatric Research Foundation, Inc"],["dc.relation.issn","0031-3998"],["dc.title","Dexamethasone increases hippocampal neuronal apoptosis in a rabbit model of Escherichia coli meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3342"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Journal of Clinical Microbiology"],["dc.bibliographiccitation.lastpage","3345"],["dc.bibliographiccitation.volume","42"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Lis, A."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Reinert, R. R."],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T10:47:43Z"],["dc.date.available","2018-11-07T10:47:43Z"],["dc.date.issued","2004"],["dc.description.abstract","Production and release of the pneumococcal virulence factors pneumolysin and lipoteichoic and teichoic acid in 75 clinical isolates were investigated. No difference was found between strains causing systemic infection or localized respiratory infection and isolates from asymptomatic carriers. This suggests that the presence of pneumolysin and lipoteichoic and teichoic acid is a necessary but not a sufficient condition for pneumococcal infection and development of invasive disease."],["dc.identifier.doi","10.1128/JCM.42.7.3342-3345.2004"],["dc.identifier.isi","000222672100081"],["dc.identifier.pmid","15243112"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48029"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Microbiology"],["dc.relation.issn","0095-1137"],["dc.title","Differences in clinical manifestation of Streptococcus pneumoniae infection are not correlated with in vitro production and release of the virulence factors pneumolysin and lipoteichoic and teichoic acids"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1450"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","1460"],["dc.bibliographiccitation.volume","91"],["dc.contributor.author","Böttcher, Tobias"],["dc.contributor.author","Ren, Hao"],["dc.contributor.author","Goiny, Michel"],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Lykkesfeldt, Jens"],["dc.contributor.author","Kuhnt, Ulrich"],["dc.contributor.author","Lotz, Miriam"],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Werner, Carola"],["dc.contributor.author","Schau, Ingmar"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Christen, Stephan"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2018-11-07T10:43:30Z"],["dc.date.available","2018-11-07T10:43:30Z"],["dc.date.issued","2004"],["dc.description.abstract","In animal models of Streptococcus pneumoniae meningitis, rifampin is neuroprotective in comparison to ceftriaxone. So far it is not clear whether this can be generalized for other protein synthesis-inhibiting antimicrobial agents. We examined the effects of the bactericidal protein synthesis-inhibiting clindamycin (n = 12) on the release of proinflammatory bacterial components, the formation of neurotoxic compounds and neuronal injury compared with the standard therapy with ceftriaxone (n = 12) in a rabbit model of pneumococcal meningitis. Analysis of the CSF and histological evaluation were combined with microdialysis from the hippocampal formation and the neocortex. Compared with ceftriaxone, clindamycin reduced the release of lipoteichoic acids from the bacteria (p = 0.004) into the CSF and the CSF leucocyte count (p = 0.011). This led to lower extracellular concentrations of hydroxyl radicals (p = 0.034) and glutamate (p = 0.016) in the hippocampal formation and a subsequent reduction of extracellular glycerol levels (p = 0.018) and neuronal apoptosis in the dentate gyrus (p = 0.008). The present data document beneficial effects of clindamycin compared with ceftriaxone on various parameters linked with the pathophysiology of pneumococcal meningitis and development of neuronal injury. This study suggests neuroprotection to be a group effect of bactericidal protein synthesis-inhibiting antimicrobial agents compared with the standard therapy with beta-lactam antibiotics in meningitis."],["dc.description.sponsorship","NINDS NIH HHS [R01 NS33997]"],["dc.identifier.doi","10.1111/j.1471-4159.2004.02837.x"],["dc.identifier.isi","000226115900020"],["dc.identifier.pmid","15584921"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47067"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0022-3042"],["dc.title","Clindamycin is neuroprotective in experimental Streptococcus pneumoniae meningitis compared with ceftriaxone"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1575"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Journal of Neuroscience Research"],["dc.bibliographiccitation.lastpage","1579"],["dc.bibliographiccitation.volume","84"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Baake, Daniel"],["dc.contributor.author","Hanssen, Mareike"],["dc.contributor.author","Huether, Gerald"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2018-11-07T08:58:05Z"],["dc.date.available","2018-11-07T08:58:05Z"],["dc.date.issued","2006"],["dc.description.abstract","Neuronal injury is frequent in bacterial meningitis, resulting in a high rate of death and neurological sequelae. In a search of potential neuroprotective strategies for treatment of bacterial meningitis, the antioxidant melatonin was neuroprotective in cell culture experiments and in a rabbit Streptococcus pneumoniae meningitis model, when treatment was started at the time of infection. In the present study, adjunctive melatonin treatment applied from the beginning of antibiotic therapy 12 hr after infection at a dose of 1.67 mg/kg/hr resulted in plasma concentrations of 451 +/- 198 ng/ml, cerebrospinal fluid (CSF) concentrations of 154 +/- 57 ng/ml and a CSF-to-plasma ratio of 0.38 +/- 0.19 (mean +/- SD). Melatonin therapy had anti inflammatory effects but did not reduce neuronal injury in either a rabbit model of gram-positive Streptococcus pneumoniae or gram-negative Escherichia coli meningitis. (c) 2006 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/jnr.21055"],["dc.identifier.isi","000242013300018"],["dc.identifier.pmid","16998917"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23557"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0360-4012"],["dc.title","Antiinflammatory but no neuroprotective effects of melatonin under clinical treatment conditions in rabbit models of bacterial meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","680"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Pediatric Research"],["dc.bibliographiccitation.lastpage","683"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Hanssen, Mareike"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2018-11-07T10:50:02Z"],["dc.date.available","2018-11-07T10:50:02Z"],["dc.date.issued","2007"],["dc.description.abstract","Despite effective antibiotic treatment, neuronal injury is frequent among children and adults with bacterial meningitis resulting in a high rate of death and neurologic sequelae. The hematopoietic cytokine erythropoietin (EPO) provides neuroprotection in models of acute and chronic neurologic diseases. We studied whether recombinant EPO (rEPO) reduces neuronal damage in a rabbit model of Escherichia coli meningitis. Inflammation within the central nervous system (CNS) was monitored by measurement of bacterial load, pleocytosis, protein, and lactate in the cerebrospinal fluid (CSF). Neuronal damage was measured by quantification of the density of apoptotic neurons in the hippocampal dentate gyrus and the concentration of the global neuronal destruction marker neuronspecific enolase (NSE) in CSF. To increase clinical relevance, rEPO was applied as adjunctive therapy from the beginning of antibiotic therapy 12 h after infection. EPO treatment applied as an intravenous injection at a dose of 1000 IU/kg body weight resulted in plasma concentrations of 6993 +/- 1406 mIU/mL, CSF concentrations of 1291 +/- 568 mIU/mL, and a CSF-to-plasma ratio of 0.18 +/- 0.07 (mean +/- SD) 6 h after injection. Under these treatment conditions, no antiinflammatory or neuroprotective effect of EPO was observed."],["dc.identifier.isi","000251104900008"],["dc.identifier.pmid","17957150"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48568"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Int Pediatric Research Foundation, Inc"],["dc.relation.issn","0031-3998"],["dc.title","No neuroprotective effect of erythropoietin under clinical treatment conditions in a rabbit model of Escherichia coli meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","74"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Antimicrobial Chemotherapy"],["dc.bibliographiccitation.lastpage","79"],["dc.bibliographiccitation.volume","59"],["dc.contributor.author","Herrmann, Isabel"],["dc.contributor.author","Kellert, Markus"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Prinz, Marco R."],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2018-11-07T11:06:47Z"],["dc.date.available","2018-11-07T11:06:47Z"],["dc.date.issued","2007"],["dc.description.abstract","Objectives: Experimental autoimmune encephalomyelitis (EAE), the animal model of multiple sclerosis (MS), can be aggravated by a mild Streptococcus pneumoniae infection. This study was performed to assess whether treatment with antibiotics inhibiting bacterial protein synthesis reduces the detrimental effect of infection on the course of EAE. Methods: In vitro, release of proinflammatory pneumococcal products was studied by enzyme immunoassay and western blot. Seven days after induction of EAE (prior to the onset of symptoms) mice were infected intraperitoneally with S. pneumoniae and treated either with the inhibitors of bacterial protein synthesis minocycline or rifampicin, or with the beta-lactam ceftriaxone. Results: During bacterial killing in vitro, minocycline and rifampicin released lower quantities of proinflammatory bacterial products from S. pneumoniae than ceftriaxone. Mice treated with minocycline developed symptoms of EAE 1 day later than mice treated with ceftriaxone. Neither minocycline nor rifampicin therapy, however, reduced the severity of EAE in comparison with ceftriaxone treatment. Conclusions: Although statistically significant (P = 0.04), a delay of 1 day in the onset of symptoms of EAE after minocycline treatment is of minor clinical relevance. These data do not support the hypothesis of superiority of a bacterial protein synthesis inhibitor over a beta-lactam antibiotic for the treatment of concomitant infections during the latent phase of EAE or MS."],["dc.identifier.doi","10.1093/jac/dkl446"],["dc.identifier.isi","000243069600010"],["dc.identifier.pmid","17079237"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52399"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0305-7453"],["dc.title","Minocycline delays but does not attenuate the course of experimental autoimmune encephalomyelitis in Streptococcus pneumoniae-infected mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","201"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neuroscience Letters"],["dc.bibliographiccitation.lastpage","204"],["dc.bibliographiccitation.volume","338"],["dc.contributor.author","Bottcher, T."],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Azeh, I."],["dc.contributor.author","Nau, R."],["dc.contributor.author","Gerber, Joachim"],["dc.date.accessioned","2018-11-07T10:40:07Z"],["dc.date.available","2018-11-07T10:40:07Z"],["dc.date.issued","2003"],["dc.description.abstract","Matrix metalloproteinase-9 (MMP-9) appears to contribute to blood-brain barrier damage and neuronal injury in bacterial meningitis. To further explore the function of MMP-9 in meningeal inflammation, we injected 104 colony forming units (CFU) of a Streptoccocus pneumoniae type 3 strain into the right forebrain of MMP-9 deficient mice (MMP-9(-/-), n = 16) and wild-type controls (129 x B6, n = 15). The clinical course of the disease, leukocyte recruitment into the subarachnoid space and bacterial titers in the brain did not differ. Yet, clearance of the bacteria from blood (log CFU/ml 4.7 [3.8/5.4] vs. 3.6 [3.0/4.0]; P = 0.005) and spleen homogenates (log CFU/ml 5.3 [4.8/5.5] vs. 4.0 [2.8/4.7]; P = 0.01) was reduced in MMP-9 deficient mice. A reduced systemic bacterial clearance of MMP-9(-/-) mice was confirmed in experimental S. pneumoniae peritonitis/sepsis. This implies a compromised systemic, but not intracerebral host response against S. pneumoniae in MMP-9 deficiency. (C) 2002 Published by Elsevier Science Ireland Ltd."],["dc.identifier.doi","10.1016/S0304-3940(02)01406-4"],["dc.identifier.isi","000181076000007"],["dc.identifier.pmid","12581831"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/46220"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Sci Ireland Ltd"],["dc.relation.issn","0304-3940"],["dc.title","Matrix metalloproteinase-9 deficiency impairs host defense mechanisms against Streptococcus pneumoniae in a mouse model of bacterial meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2649"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Antimicrobial Agents and Chemotherapy"],["dc.bibliographiccitation.lastpage","2654"],["dc.bibliographiccitation.volume","47"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Kerstan, H."],["dc.contributor.author","Bottcher, T."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Siemer, A."],["dc.contributor.author","Zysk, G."],["dc.contributor.author","Mitchell, Timothy J."],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T10:37:04Z"],["dc.date.available","2018-11-07T10:37:04Z"],["dc.date.issued","2003"],["dc.description.abstract","Pneumolysin, a virulence factor of Streptococcus pneumoniae with cytotoxic and proinflammatory activities, occurs at concentrations from 0.85 to 180 ng/ml in cerebrospinal fluid (CSF) of meningitis patients. In pneumococcal cultures and in a rabbit meningitis model, the concentrations of pneumolysin in supernatant and CSF were lower after addition of nonbacteriolytic bactericidal antibiotics (rifampin and clindamycin) than after incubation with ceftriaxone."],["dc.identifier.doi","10.1128/AAC.47.8.2649-2654.2003"],["dc.identifier.isi","000184449800041"],["dc.identifier.pmid","12878534"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45477"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Microbiology"],["dc.relation.issn","0066-4804"],["dc.title","Reduced release of pneumolysin by Streptococcus pneumoniae in vitro and in vivo after treatment with nonbacteriolytic antibiotics in comparison to ceftriaxone"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","355"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.lastpage","368"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Stringaris, Argyris"],["dc.contributor.author","Geisenhainer, J."],["dc.contributor.author","Bergmann, F"],["dc.contributor.author","Balshusemann, C."],["dc.contributor.author","Lee, U."],["dc.contributor.author","Zysk, G"],["dc.contributor.author","Mitchell, T. J."],["dc.contributor.author","Keller, B. U."],["dc.contributor.author","Kuhnt, U."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2017-09-07T11:45:09Z"],["dc.date.available","2017-09-07T11:45:09Z"],["dc.date.issued","2002"],["dc.description.abstract","Neuronal injury in bacterial meningitis is caused by the interplay of host inflammatory responses and direct bacterial toxicity. We investigated the mechanisms by which pneumolysin, a cytosolic pneumococcal protein, induces damage to neurons. The toxicity after exposure of human SH-SY5Y neuroblastoma cells and hippocampal organotypic cultures to pneumolysin was time- and dose-dependent. Pneumolysin led to a strong calcium influx apparently mediated by pores on the cell membrane formed by the toxin itself and not by voltage-gated calcium channels. Buffering of intracellular calcium with BAPTA-AM [1; 2-bis (o-aminophenoxy) ethane N, N, N', N'-tetraacetic acid tetra(acetomethoxyl) ester] improved survival of neuronal cells following challenge with pneumolysin. Western blotting revealed increased phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) as early as 30 min after challenge with pneumolysin. SB 203580, a potent and selective inhibitor of p38 MAPK, rescued human neuronal cells from pneumolysin-induced death. Inhibition of the mitochondrial permeability transition pore using bongkrekate and caspase inhibition also improved survival following challenge with the toxin. Modulation of cell death pathways activated by pneumolysin may influence the outcome of pneumococcal meningitis. (C) 2003 Elsevier Science (USA)."],["dc.identifier.doi","10.1006/nbdi.2002.0561"],["dc.identifier.gro","3144151"],["dc.identifier.isi","000180866500001"],["dc.identifier.pmid","12586546"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1743"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.publisher.place","San diego"],["dc.relation.conference","54th Annual Meeting of the American-Academy-of-Neurology"],["dc.relation.eventlocation","DENVER, COLORADO"],["dc.relation.ispartof","Neurobiology of Disease"],["dc.relation.issn","0969-9961"],["dc.title","Neurotoxicity of pneumolysin, a major pneumococcal virulence factor, involves calcium influx and depends on activation of p38 mitogen-activated protein kinase"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","806"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Neuropathology & Experimental Neurology"],["dc.bibliographiccitation.lastpage","815"],["dc.bibliographiccitation.volume","64"],["dc.contributor.author","Tauber, Simone C."],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.contributor.author","Nau, R."],["dc.contributor.author","Gerber, Joachim"],["dc.date.accessioned","2018-11-07T10:56:19Z"],["dc.date.available","2018-11-07T10:56:19Z"],["dc.date.issued","2005"],["dc.description.abstract","Proliferation and differentiation of neural progenitor cells is increased after bacterial meningitis. To identify endogenous factors involved in neurogenesis, expression of brain-derived neurotrophic factor (BDNF), TrkB, nerve growth factor (NGF), and glial cell line-derived neurotrophic factor (GDNF) was investigated. C57BL/6 mice were infected by intracerebral injection of Streptococcus pneumoniae. Mice were killed 30 hours later or treated with ceftriaxone and killed 4 days after infection. Hippocampal BDNF mRNA levels were increased 2.4-fold 4 days after infection (p = 0.026). Similarly, BDNF protein levels in the hippocampal formation were higher in infected mice than in control animals (p = 0.0003). This was accompanied by an elevated proliferation of dentate granule cells (p = 0.0002). BDNF protein was located predominantly in the hippocampal CA3/4 area and the hilus of the dentate gyrus. The density of dentate granule cells expressing the BDNF receptor TrkB as well as mRNA levels of TrkB in the hippocampal formation were increased 4 days after infection (p = 0.027 and 0.0048, respectively). Conversely, NGF mRNA levels at 30 hours after infection were reduced by approximately 50% (p = 0.004). No significant changes in GDNF expression were observed. In conclusion, increased synthesis of BDNF and TrkB suggests a contribution of this neurotrophic factor to neurogenesis after bacterial meningitis."],["dc.identifier.doi","10.1097/01.jnen.0000178853.21799.88"],["dc.identifier.isi","000231781300009"],["dc.identifier.pmid","16141791"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49984"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.eissn","1554-6578"],["dc.relation.issn","0022-3069"],["dc.title","Increased expression of BDNF and proliferation of dentate granule cells after bacterial meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]