Nau, Roland

[["dc.bibliographiccitation.firstpage","1877"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Journal of Neuroscience Research"],["dc.bibliographiccitation.lastpage","1883"],["dc.bibliographiccitation.volume","87"],["dc.contributor.author","Tauber, Simone C."],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Schulz, Daniela"],["dc.contributor.author","Kellert, Benedikt"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Gerber, Joachim"],["dc.date.accessioned","2018-11-07T08:29:27Z"],["dc.date.available","2018-11-07T08:29:27Z"],["dc.date.issued","2009"],["dc.description.abstract","An increase in adult neurogenesis was observed after exposure to enriched environment (EE) and during reconvalescence from experimental pneumococcal meningitis. This study investigated neurogenesis and spatial learning performance 5 weeks after bacterial meningitis and exposure to EE. C57BL/6 mice were infected by intracerebral injection of Streptococcus pneumoniae and treated with ceftriaxone for 5 days. Forty-eight hours after infection, one group (n = 22) was exposed to EE and the other group (n = 23) housed under standard conditions. Another set of mice was kept under either enriched (n = 16) or standard (n = 15) conditions without bacterial meningitis. Five weeks later, the Morris water maze was performed, and neurogenesis was evaluated by means of immunohistochemistry. Mice housed in EE without prior bacterial infection displayed both increased neurogenesis and improved water maze performance in comparison with uninfected control animals. Bacterial meningitis stimulated neurogenesis in the granular cell layer of the dentate gyrus: with standard housing conditions, we observed a higher density of BrdU-immunolabeled and TUC-4-expressing cells 5 weeks after induction of bacterial meningitis than in the noninfected control group. EE did not further increase progenitor cell proliferation and neuronal differentiation in the subgranular cell layer of the dentate gyrus after bacterial meningitis in comparison with infected mice housed under standard conditions. Moreover, the Morris water maze showed no significant differences between survivors of meningitis exposed to EE and animals kept in standard housing. In summary, exposure to EE after pneumococcal meningitis did not further increase meningitis-induced neurogenesis or improve spatial learning. (C) 2009 Wiley-Liss, Inc."],["dc.description.sponsorship","Else Kroner-Fresenius-Stiftung [1161/06//A70/06]"],["dc.identifier.doi","10.1002/jnr.22010"],["dc.identifier.isi","000265462800015"],["dc.identifier.pmid","19170185"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16657"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0360-4012"],["dc.title","Enriched Environment Fails To Increase Meningitis-Induced Neurogenesis and Spatial Memory in a Mouse Model of 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","30"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","39"],["dc.bibliographiccitation.volume","113"],["dc.contributor.author","Schmidt, H"],["dc.contributor.author","Tlustochowska, A."],["dc.contributor.author","Stuertz, K."],["dc.contributor.author","Djukic, M."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Schutz, Ekkehard"],["dc.contributor.author","Kuhnt, U."],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2021-06-01T10:50:09Z"],["dc.date.available","2021-06-01T10:50:09Z"],["dc.date.issued","2001"],["dc.description.abstract","Hippocampal slices of newborn rats were exposed to either heat-inactivated Streptococcus pneumoniae R6 (hiR6) equivalent to 10(6) and 10(8) CFU/ml, lipoteichoic acid (LTA) (0.3 mug/ml and 30 mug/ml), peptidoglycans (PG) (0.3, 30, 50 and 100 mug/ml), pneumococcal DNA (pDNA) (0.3 and 30 mug/ml) or medium only (control). Cell injury was examined by Nissl staining, Annexin V and NeuN immunohistochemistry, and quantified by propidium iodide (PI) uptake and by determining neuron-specific enolase (NSE) concentration in the culture medium. Necrotic and apoptotic cell damage occurred in all treatment groups. Overall damage (Nissl and PI staining) was most prominent after hiR6 (10(8) CFU/ml), followed by LTA (30 mug/ml), pDNA (30 mug/ml), and not detectable after PG (30 mug/ml) exposure. PG (100 mug/ml) induced severe damage. Apoptotic cells were most frequent after exposure to LTA and hiR6. Damage in the neuronal cell layers (NeuN, NSE) was most severe after treatment with hiR6 (10(8) CFU/ml), followed by PG (100 mug/ml), pDNA (30 mug/ml), and LTA (30 mug/ml). (C) 2001 Elsevier Science B.V. All rights reserved."],["dc.identifier.doi","10.1016/S0165-5728(00)00402-1"],["dc.identifier.isi","000166575000004"],["dc.identifier.pmid","11137574"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86547"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0165-5728"],["dc.title","Organotypic hippocampal cultures A model of brain tissue damage in Streptococcus pneumoniae meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","809"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","European Journal of Endocrinology"],["dc.bibliographiccitation.lastpage","816"],["dc.bibliographiccitation.volume","143"],["dc.contributor.author","Michel, W."],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Schneider, O."],["dc.contributor.author","Shintani, Y."],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Smirnov, Alexey"],["dc.contributor.author","Stringaris, A. K."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T10:33:22Z"],["dc.date.available","2018-11-07T10:33:22Z"],["dc.date.issued","2000"],["dc.description.abstract","Objective: Follistatin (FS) is the specific binding protein of activin and expression of both factors is regulated by inflammatory agents. Therefore. FS concentrations were determined in cerebrospinal fluid (CSF) of patients with bacterial and viral meningitis or multiple sclerosis (MS), as well as in the CSF of patients without meningial inflammation or autoimmune diseases. Furthermore, a mouse pneumococcal meningitis model was used to localise the cellular sources of FS in brains of normal and meningitic mice. Methods: FS concentrations in CSF were determined by ELISA; FS in mice was localised by in situ hybridisation and immunohistochemistry. Results: FS concentrations were greater than or equal to0.4 mug/l in 22 of 66 CSF samples of meningitis patients versus 2 of 27 CSF samples from patients with multiple sclerosis (P < 0.05) and 2 of 41 CSF specimen from patients without neuroinflammatory diseases (P < 0.01). In the CSF of patients with meningitis, the concentration of FS was correlated with total protein (P < 0.005) and lactate concentrations (P < 0.05), but not with leukocyte counts, interval between onset of disease and CSF analysis, or clinical outcome. The CSF-to-serum ratios of FS and albumin also correlated significantly (P < 0.0005). in some patients with meningitis the CSF-to-serum ratios suggested that the elevated FS in CSF did not originate from serum alone. FS was localised in mice brains to neurones of the hippocampus, dentate gyrus, neocortex, and to the choroid plexus. Analyses of brains and other organs from uninfected and infected animals sacrificed 6-36 h after infection did not reveal any obvious differences in the distribution and intensity of FS mRNA and protein expression. Conclusions: The concentration of FS in humans is elevated during meningitis. In some patients the increase is caused by a release of FS from brain into CSF. Data from the mouse meningitis model suggest that increased CSF concentrations of FS in meningitis appear not to be accompanied by an elevated number of cells containing FS mRNA or protein in the brain."],["dc.identifier.isi","000166654700013"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44594"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Bioscientifica Ltd"],["dc.relation.issn","0804-4643"],["dc.title","Follistatin (FS) in human cerebrospinal fluid and regulation of FS expression in a mouse model of meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","509"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","511"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Nau, R."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.date.accessioned","2018-11-07T10:51:11Z"],["dc.date.available","2018-11-07T10:51:11Z"],["dc.date.issued","2004"],["dc.description.abstract","The contribution of axonal injury to CNS damage in bacterial meningitis was studied by histology and immunohistochemistry for amyloid-beta precursor protein in humans and experimental rabbits. Axonal injury in the white matter caused predominantly but not exclusively by ischemia was detected in all autopsy cases (n = 5) and in 11 of 15 brains of rabbits 18 to 24 hours after intracisternal infection with Streptococcus pneumoniae. This suggests a substantial contribution of axonal pathology to neurologic sequelae after bacterial meningitis."],["dc.identifier.isi","000189238800038"],["dc.identifier.pmid","14872046"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48830"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0028-3878"],["dc.title","Axonal injury, a neglected cause of CNS damage in 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","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","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","289"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","298"],["dc.bibliographiccitation.volume","94"],["dc.contributor.author","Lotz, M."],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Esselmann, Herrmann"],["dc.contributor.author","Iliev, Asparouh I."],["dc.contributor.author","Prinz, Marco R."],["dc.contributor.author","Wiazewicz, N."],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T09:20:41Z"],["dc.date.available","2018-11-07T09:20:41Z"],["dc.date.issued","2005"],["dc.description.abstract","The interaction of endogenous and exogenous stimulators of innate immunity was examined in primary cultures of mouse microglial cells and macrophages after application of defined Toll-like receptor (TLR) agonists [lipopolysaccharide (LPS) (TLR4), the synthetic lipopeptide Pam3Cys-Ser-Lys4 (Pam3Cys) (TLR2) and single-stranded unmethylated CpG-DNA (CpG) (TLR9)] alone and in combination with amyloid beta peptide (Abeta) 1-40. Abeta 1-40 stimulated microglial cells and macrophages primed by interferon-gamma in a dose-dependent manner. Co-administration of Abeta1-40 with LPS or Pam3Cys led to an additive release of nitric oxide (NO) and tumour necrosis factor alpha (TNF-alpha). This may be one reason for the clinical deterioration frequently observed in patients with Alzheimer's disease during infections. In contrast, co-application of Abeta1-40 with CpG led to a substantial decrease of NO and TNF- alpha release compared with stimulation with CpG alone. Abeta 1-40 and CpG did not co-localize within the same subcellular compartment, making a direct physicochemical interaction as the cause of the observed antagonism very unlikely. This suggests that not all TLR agonists enhance the stimulatory effect of Abeta on innate immunity."],["dc.identifier.doi","10.1111/j.1471-4159.2005.03188.x"],["dc.identifier.isi","000230289200001"],["dc.identifier.pmid","15998280"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28935"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1471-4159"],["dc.relation.issn","0022-3042"],["dc.title","Amyloid beta peptide 1-40 enhances the action of Toll-like receptor-2 and -4 agonists but antagonizes Toll-like receptor-9-induced inflammation in primary mouse microglial cell cultures"],["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","87"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","96"],["dc.bibliographiccitation.volume","159"],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Bader, Samuel"],["dc.contributor.author","Muhlhauser, F."],["dc.contributor.author","Brechtel, K."],["dc.contributor.author","Mitchell, Timothy J."],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T08:28:47Z"],["dc.date.available","2018-11-07T08:28:47Z"],["dc.date.issued","2005"],["dc.description.abstract","Microglial cells express Toll-like receptors (TLRs) recognising exogenous and endogenous ligands. Upon stimulation with agonists of TLR2, TLR4, and TLR9, nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha) were released by primary mouse microglial cell cultures. Endotoxin was most potent in stimulating microglia followed by pneumolysin, cytosine-guanosine (CpG) oligodesoxynucleotide (ODN), and Tripalmitoyl-S-glycetyl-cysteine. Maximum stimulation of TLR2, TLR4, and TLR9 resulted in approximately equal amounts of nitric oxide release. Pneumolysin was a potent activator of microglial cells; at high concentrations, it reduced cell viability. No cytotoxicity was noted with the other TLR agonists. Costimulation with maximum concentrations of two TLR agonists did not further increase nitric oxide release. Costimulation with submaximum concentrations was additive or supraadditive, suggesting that even low concentrations of products of infectious agents can lead to microglial activation via TLRs. (C) 2004 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jneuroim.2004.10.005"],["dc.identifier.isi","000226882300010"],["dc.identifier.pmid","15652406"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16503"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1872-8421"],["dc.relation.issn","0165-5728"],["dc.title","Dose-dependent activation of microglial cells by Toll-like receptor agonists alone and in combination"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]