Bunkowski, Stephanie

[["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","865"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Infection and Immunity"],["dc.bibliographiccitation.lastpage","871"],["dc.bibliographiccitation.volume","78"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Agarwal, Amit"],["dc.contributor.author","Tauber, Simone C."],["dc.contributor.author","Czesnik, Dirk"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Hammerschmidt, Sven"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2018-11-07T08:46:16Z"],["dc.date.available","2018-11-07T08:46:16Z"],["dc.date.issued","2010"],["dc.description.abstract","Toll-like receptors (TLRs) are crucial pattern recognition receptors in innate immunity that are expressed in microglia, the resident macrophages of the brain. TLR2, -4, and -9 are important in the responses against Streptococcus pneumoniae, the most common agent causing bacterial meningitis beyond the neonatal period. Murine microglial cultures were stimulated with agonists for TLR1/2 (Pam3CSK4), TLR4 (lipopolysaccharide), and TLR9 (CpG oligodeoxynucleotide) for 24 h and then exposed to either the encapsulated D39 (serotype 2) or the nonencapsulated R6 strain of S. pneumoniae. After stimulation, the levels of interleukin-6 and CCL5 (RANTES [regulated upon activation normal T-cell expressed and secreted]) were increased, confirming microglial activation. The TLR1/2, -4, and -9 agonist-stimulated microglia ingested significantly more bacteria than unstimulated cells (P < 0.05). The presence of cytochalasin D, an inhibitor of actin polymerizaton, blocked >90% of phagocytosis. Along with an increased phagocytic activity, the intracellular bacterial killing was also increased in TLR-stimulated cells compared to unstimulated cells. Together, our data suggest that microglial stimulation by these TLRs may increase the resistance of the brain against pneumococcal infections."],["dc.identifier.doi","10.1128/IAI.01110-09"],["dc.identifier.isi","000273855600033"],["dc.identifier.pmid","19933834"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20648"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Microbiology"],["dc.relation.issn","0019-9567"],["dc.title","Toll-Like Receptor Stimulation Enhances Phagocytosis and Intracellular Killing of Nonencapsulated and Encapsulated Streptococcus pneumoniae by Murine Microglia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","329"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Brain Pathology"],["dc.bibliographiccitation.lastpage","336"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Nau, R."],["dc.contributor.author","Haase, S."],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.date.accessioned","2018-11-07T10:19:42Z"],["dc.date.available","2018-11-07T10:19:42Z"],["dc.date.issued","2002"],["dc.description.abstract","Apoptosis of dentate granule cells is a typical feature of several animal models of disease. In 20 autopsy cases of subarachnoid hemorrhage (SAH) and global cerebral hypoxia caused by protracted shock or respiratory failure, we evaluated by light microscopy and in situ tailing whether this pattern of neuronal damage also occurs in humans. In subarachnoid hemorrhage, 4.0/mm(2) (0-13.0/mm(2)) apoptotic neurons were observed in the dentate gyrus, in cerebral hypoxia 3.6/mm(2) (0-19.9/mm(2)) (p>0.05), and in 10 aged-matched control cases dying rapidly from non-neurological diseases 0/mm(2) (0-0/mm(2)) (median [range]) (p<0.001 versus SAH and hypoxia). Neuronal apoptosis in the dentate gyrus was most frequent, when death occurred later than 24 hours and less than 11 days after disease onset. Neuronal damage in the hippocampus was always necrotic. It was more severe in hypoxia than in SAH (median neuronal damage score 3 [range: 0-3] versus 0 [0-3], P<0.001). Apoptosis appears to be the predominant mechanism of death in dentate granule cells irrespective of the underlying disease, whereas neuronal death in the hippocampus generally is of necrotic morphology."],["dc.identifier.isi","000176772800006"],["dc.identifier.pmid","12146801"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41717"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Int Soc Neuropathology"],["dc.relation.issn","1015-6305"],["dc.title","Neuronal apoptosis in the denate gyrus in humans with subarachnoid hemorrage and cerebral hypoxia"],["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.artnumber","15"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Fluids and Barriers of the CNS"],["dc.bibliographiccitation.lastpage","5"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Djukic, Marija"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Lange, Peter"],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2017-09-07T11:44:33Z"],["dc.date.available","2017-09-07T11:44:33Z"],["dc.date.issued","2016"],["dc.description.abstract","Background The composition of the cerebrospinal fluid (CSF) is not homogeneous, and concentrations of proteins from different origins diverge among ventricular, cisternal and lumbar CSF fractions. Concentrations of blood-derived proteins increase and of brain-derived proteins decrease from ventricular to lumbar fractions. We studied whether the origin of the CSF portion analysed may affect results in CSF analysis for dementia. Methods In 16 geriatric patients with suspected normal pressure hydrocephalus [age 82.5 (76/87) years; median (25th/75th percentile)] a lumbar spinal tap of 40 ml was performed. The CSF was sequentially collected in 8 fractions of 5 ml with the 1st fraction corresponding to lumbar CSF, the 8th to cisterna magna-near CSF. Fractions were analysed for total protein, albumin, Tau protein (Tau), phosphorylated Tau (pTau), Amyloid beta 1–42 (Aβ1–42), Amyloid beta 1–40 (Aβ1–40), and the Aβ1–42/Aβ1–40 ratio. Results The concentrations of total protein and albumin increased from cisternal to lumbar fractions due to diffusion-related accumulation from blood to CSF with significantly higher concentrations in fraction 1 compared to fraction 8. The concentrations of Tau showed a non-significant trend towards decreased values in lumbar samples, and pTau was slightly, but significantly decreased in the lumbar fraction 1 [26.5 (22.5/35.0) pg/ml] compared to the cistern-near fraction 8 [27.0 (24.2/36.3) pg/ml] (p = 0.02, Wilcoxon signed rank test). Aβ1-42, Aβ1-40, and the Aβ1-42/Aβ1-40 ratio remained almost constant. Conclusions According to the flow-related diverging dynamics of blood-derived and brain-derived proteins in CSF, the concentrations of Tau and pTau tended to be lower in lumbar compared to cisternal CSF fractions after a spinal tap of 40 ml. The differences reached statistical significance for pTau only. The small differences will not affect clinical interpretation of markers of dementia in the vast majority of cases."],["dc.identifier.doi","10.1186/s12987-016-0039-9"],["dc.identifier.gro","3151687"],["dc.identifier.pmid","27581842"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13876"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8505"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","2045-8118"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Small cisterno-lumbar gradient of phosphorylated Tau protein in geriatric patients with suspected normal pressure hydrocephalus"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["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","121"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","129"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Werner, Katharina"],["dc.contributor.author","Bitsch, Annette"],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.date.accessioned","2018-11-07T09:59:34Z"],["dc.date.available","2018-11-07T09:59:34Z"],["dc.date.issued","2002"],["dc.description.abstract","The activation of macrophages/microglia in multiple sclerosis (MS) lesions plays a central role in the effector phase of myelin breakdown. The precise patterns of macrophage/microglia activation during demyelination have not yet been defined. The growth and activating factor macrophage-colony stimulating factor (M-CSF) and its specific receptor (M-CSFR) may be involved in this process. The present study investigated the expression of M-CSF and M-CSFR mRNA by in situ hybridization in 60 lesions from 32 MS patients. In the control and periplaque white matter, microglia was almost completely M-CSFR positive. Irrespective of the demyelinating activity, an increased number of cells expressed M-CSF or M-CSFR mRNA within the lesions. However, despite the tremendous increase in macrophages/microglia within the lesions, the relative number of these cells expressing M-CSF or M-CSFR decreased. There was no correlation of M-CSF or M-CSFR expression with active myelin breakdown. The correlation between the clinical course and the expression of M-CSF or M-CSFR mRNA revealed significant differences with the lowest expression in primary progressive MS. These results suggest a downregulation of M-CSF and M-CSFR inside the MS plaque probably due to the high amount of macrophage-derived cytokines or mediators. Nevertheless, the differences in the relative number of cells expressing the M-CSF/M-CSFR pathway implicate that this pathway may be an important contributory factor in different forms of MS pathology. (C) 2002 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/glia.10120"],["dc.identifier.isi","000178364300011"],["dc.identifier.pmid","12237849"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37618"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0894-1491"],["dc.title","The relative number of macrophages/microglia expressing macrophage colony-stimulating factor and its receptor decreases in multiple sclerosis lesions"],["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","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","861"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Neuropathology & Experimental Neurology"],["dc.bibliographiccitation.lastpage","867"],["dc.bibliographiccitation.volume","80"],["dc.contributor.author","Seele, Jana"],["dc.contributor.author","Ballüer, Melissa"],["dc.contributor.author","Tauber, Simone C"],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Schulz, Katja"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Beineke, Andreas"],["dc.contributor.author","Pägelow, Dennis"],["dc.contributor.author","Fulde, Marcus"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2021-12-01T09:23:50Z"],["dc.date.available","2021-12-01T09:23:50Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract To improve the therapy of neonatal central nervous system infections, well-characterized animal models are urgently needed. The present study analyzes neuropathological alterations with particular focus on neural injury and repair in brains of neonatal mice with Listeria monocytogenes (LM) meningitis/meningoencephalitis using a novel nasal infection model. The hippocampal formation and frontal cortex of 14 neonatal mice with LM meningitis/meningoencephalitis and 14 uninfected controls were analyzed by histology, immunohistochemistry, and in situ tailing for morphological alterations. In the dentate gyrus of the hippocampal formation of mice with LM meningitis/meningoencephalitis, an increased density of apoptotic neurons visualized by in situ tailing (p = 0.04) and in situ tailing plus immunohistochemistry for activated Caspase-3 (p < 0.0001) was found. A decreased density of dividing cells stained with an anti-PCNA-antibody (p < 0.0001) and less neurogenesis visualized by anti-calretinin (p < 0.0001) and anti-calbindin (p = 0.01) antibodies were detected compared to uninfected controls. The density of microglia was higher in LM meningitis (p < 0.0001), while the density of astrocytes remained unchanged. Infiltrating monocytes and neutrophilic granulocytes likely contributed to tissue damage. In conclusion, in the brains of LM-infected mice a strong immune response was observed which led to neuronal apoptosis and an impaired neural regeneration. This model appears very suitable to study therapies against long-term sequelae of neonatal LM meningitis."],["dc.description.abstract","Abstract To improve the therapy of neonatal central nervous system infections, well-characterized animal models are urgently needed. The present study analyzes neuropathological alterations with particular focus on neural injury and repair in brains of neonatal mice with Listeria monocytogenes (LM) meningitis/meningoencephalitis using a novel nasal infection model. The hippocampal formation and frontal cortex of 14 neonatal mice with LM meningitis/meningoencephalitis and 14 uninfected controls were analyzed by histology, immunohistochemistry, and in situ tailing for morphological alterations. In the dentate gyrus of the hippocampal formation of mice with LM meningitis/meningoencephalitis, an increased density of apoptotic neurons visualized by in situ tailing (p = 0.04) and in situ tailing plus immunohistochemistry for activated Caspase-3 (p < 0.0001) was found. A decreased density of dividing cells stained with an anti-PCNA-antibody (p < 0.0001) and less neurogenesis visualized by anti-calretinin (p < 0.0001) and anti-calbindin (p = 0.01) antibodies were detected compared to uninfected controls. The density of microglia was higher in LM meningitis (p < 0.0001), while the density of astrocytes remained unchanged. Infiltrating monocytes and neutrophilic granulocytes likely contributed to tissue damage. In conclusion, in the brains of LM-infected mice a strong immune response was observed which led to neuronal apoptosis and an impaired neural regeneration. This model appears very suitable to study therapies against long-term sequelae of neonatal LM meningitis."],["dc.identifier.doi","10.1093/jnen/nlab079"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94770"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.eissn","1554-6578"],["dc.relation.issn","0022-3069"],["dc.rights.uri","https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model"],["dc.title","Neural Injury and Repair in a Novel Neonatal Mouse Model of Listeria Monocytogenes Meningoencephalitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]