Spreer, Annette

[["dc.bibliographiccitation.firstpage","126"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Dementia and Geriatric Cognitive Disorders"],["dc.bibliographiccitation.lastpage","134"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Fronek, Kathrin"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Lange, Peter"],["dc.date.accessioned","2018-11-07T08:51:09Z"],["dc.date.available","2018-11-07T08:51:09Z"],["dc.date.issued","2011"],["dc.description.abstract","Background/Aims: Determination of marker proteins of neuronal degeneration in cerebrospinal fluid (CSF) is of increasing importance. However, preanalytical problems may compromise the results. Methods: We studied the influence of the transport tube material and shaking at room temperature on the CSF concentrations of beta-amyloid and tau protein determined by enzyme immunoassays. Results: The materials of the transport tube moderately influenced the CSF concentrations of beta-amyloid and tau protein. Polyethylene and polypropylene tubes were well suited, but glass, polycarbonate and polystyrene tubes caused a decrease in the CSF beta-amyloid and tau protein concentrations. The strongest impact, however, was caused by bacterial contamination of samples. Contamination with high concentrations of Pseudomonas aeruginosa and related species rendered beta-amyloid undetectable and strongly diminished tau protein concentrations. The effects of several Gram-positive bacteria were less pronounced. Addition of 0.1% sodium azide prior to bacterial contamination increased the interval at which CSF could be kept at room temperature without a substantial reduction of the beta-amyloid or tau protein concentration. Conclusion: Polyethylene or polypropylene tubes are suitable transport vessels for CSF samples. Bacterial contamination during sampling and portioning must be avoided. Addition of sodium azide may be an option when transport of the sample is delayed. Copyright (C) 2011 S. Karger AG, Basel"],["dc.identifier.doi","10.1159/000330912"],["dc.identifier.fs","580959"],["dc.identifier.isi","000295875400006"],["dc.identifier.pmid","21952521"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21862"],["dc.language.iso","en"],["dc.notes","This publication is with permission of the rights owner freely accessible due to an Alliance licence and a national licence (funded by the DFG, German Research Foundation) respectively."],["dc.notes.intern","Merged from goescholar"],["dc.notes.intern","In goescholar merged with http://resolver.sub.uni-goettingen.de/purl?gs-1/8159"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","S. Karger AG"],["dc.relation.eissn","1421-9824"],["dc.relation.issn","1420-8008"],["dc.rights","Goescholar"],["dc.rights.access","openAccess"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.mesh","Amyloid beta-Peptides"],["dc.subject.mesh","Cerebrospinal Fluid"],["dc.subject.mesh","Cerebrospinal Fluid Proteins"],["dc.subject.mesh","Dementia"],["dc.subject.mesh","Enzyme-Linked Immunosorbent Assay"],["dc.subject.mesh","Equipment Design"],["dc.subject.mesh","Humans"],["dc.subject.mesh","Pseudomonas aeruginosa"],["dc.subject.mesh","Quality Control"],["dc.subject.mesh","Specimen Handling"],["dc.subject.mesh","Stenotrophomonas maltophilia"],["dc.subject.mesh","tau Proteins"],["dc.title","Bacterial Contamination and the Transport Vial Material Affect Cerebrospinal Fluid Concentrations of beta-Amyloid and Tau Protein as Determined by Enzyme Immunoassay"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["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","630"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","636"],["dc.bibliographiccitation.volume","259"],["dc.contributor.author","Djukic, Marija"],["dc.contributor.author","Schmidt-Samoa, Carsten"],["dc.contributor.author","Lange, Peter"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Neubieser, Katja"],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Schmidt, Holger"],["dc.date.accessioned","2018-11-07T09:11:41Z"],["dc.date.available","2018-11-07T09:11:41Z"],["dc.date.issued","2012"],["dc.description.abstract","Presence of BB-specific antibodies in the cerebrospinal fluid (CSF) with evidence of their intrathecal production in conjunction with the white cell count in the CSF and typical clinical symptoms is the traditional diagnostic gold standard of Lyme neuroborreliosis (LNB). Few data are available on the CSF lactate concentration in European adults with the diagnosis of acute LNB. The objective of the study was to investigate the CSF changes during acute LNB. Routine CSF parameters [leukocyte count, protein, lactate and albumin concentrations, CSF/serum quotients of albumin (Q(Alb)), IgG, IgA and IgM, and oligoclonal IgG bands] and the Borrelia burgdorferi (BB)-specific antibody index were retrospectively studied in relation to the clinical presentation in patients diagnosed with acute LNB. A total of 118 patients with LNB were categorized into the following groups according to their symptoms at presentation; group 1: polyradiculoneuritis (Bannwarth's syndrome), group 2: isolated facial palsy and group 3: predominantly meningitic course of the disease. In addition to the CSF of patients with acute LNB, CSF of 19 patients with viral meningitis (VM) and 3 with neurolues (NL) were analyzed. There were 97 patients classified with definite LNB, and 21 as probable LNB. Neck stiffness and fever were reported by 15.3% of patients. Most of these patients were younger than 50 years. Polyradiculoneuritis was frequently found in patients older than 50 years. Lymphopleocytosis was found in all patients. Only 5 patients had a CSF lactate >= 3.5 mmol/l, and the mean CSF lactate level was not elevated (2.1 +/- A 0.6 mmol/l). The patients with definite LNB had significantly higher lactate levels than patients with probable LNB. Elevated lactate levels were accompanied by fever and headache. In the Reiber nomograms, intrathecal immunoglobulin synthesis was found for IgM in 70.2% followed by IgG in 19.5%. Isoelectric focussing detected an intrathecal IgG synthesis in 83 patients (70.3%). Elevated BB AIs in the CSF were found in 97 patients (82.2%). Patients with VM showed lower CSF protein concentration and CSF/serum quotients of albumin than LNB patients. In acute LNB, all patients had elevated cerebrospinal fluid (CSF) leukocyte counts. In contrast to infections by other bacteria, CSF lactate was lower than 3.5 mmol/l in all but 5 patients. The CSF findings did not differ between polyradiculoneuritis, facial palsy, and meningitis. The CSF in LNB patients strongly differed from CSF in VM patients with respect to protein concentration and the CSF/serum albumin quotient."],["dc.identifier.doi","10.1007/s00415-011-6221-8"],["dc.identifier.isi","000302489400004"],["dc.identifier.pmid","21898139"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8098"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26777"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","0340-5354"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Cerebrospinal fluid findings in adults with acute Lyme neuroborreliosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","327"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Chemotherapy"],["dc.bibliographiccitation.lastpage","331"],["dc.bibliographiccitation.volume","53"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","von Rueden, Christian"],["dc.contributor.author","Mitchell, Timothy J."],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2018-11-07T11:06:16Z"],["dc.date.available","2018-11-07T11:06:16Z"],["dc.date.issued","2007"],["dc.description.abstract","Objective: Pneumolysin is an important virulence factor of Streptococcus pneumoniae with cytotoxic and proinflammatory activities released during growth and autolysis. At concentrations above the minimal inhibitory concentration, the protein-synthesis-inhibiting antibiotics erythromycin, clindamycin and rifampicin inhibit the production and/or release of virulence factors in various bacterial species. We investigated the influence of subinhibitory concentrations of these antibiotics on production and release of pneumolysin by S. pneumoniae strain D39. Methods: The pneumococcal strain D39 was grown in broth and treated with antibiotics at a concentration of 1/32 of the respective minimal inhibitory concentration. Cytoplasmic and extracellular pneumolysin was measured by quantitative immunoblotting with recombinant pneumolysin as standard. Results: The subinhibitory antibiotic concentrations evaluated did not affect bacterial growth. During logarithmic growth, production of pneumolysin was decreased by clindamycin, erythromycin and rifampicin by approximately 50% compared with untreated controls. The release of pneumolysin was decreased to a similar extent. Conclusion: A decrease in pneumolysin production by 50% probably has a moderate biological effect. We do not advocate the use of subinhibitory concentrations of antibiotics to modulate the expression of virulence factors during pneumococcal disease, particularly with regard to the risk of development of antibiotic resistance. Copyright (C) 2007 S. Karger AG, Basel."],["dc.identifier.doi","10.1159/000107691"],["dc.identifier.isi","000249306100005"],["dc.identifier.pmid","17728540"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52264"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","0009-3157"],["dc.title","Influence of subinhibitory concentrations of protein-synthesis-inhibiting antibiotics on production and release of the pneumococcal virulence factor pneumolysin in vitro"],["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","7"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","AKTUELLE NEUROLOGIE"],["dc.bibliographiccitation.lastpage","15"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Djukic, M."],["dc.contributor.author","Nau, R."],["dc.contributor.author","Eiffert, Helmut"],["dc.date.accessioned","2018-11-07T09:28:28Z"],["dc.date.available","2018-11-07T09:28:28Z"],["dc.date.issued","2013"],["dc.description.abstract","Neuroborreliosis is a nervous system infection caused by Borrelia burgdorferi sensu lato. Lyme disease is the most frequent tick-borne infectious disease in Europe affecting the skin, joints, heart, nervous system and rarely the eyes. Since the discovery of the causative pathogen Borrelia burgdorferi 30 years ago, the rapid accumulation of knowledge about this disease has resulted in well-evaluated clinical and microbiological diagnostic guidelines. Today, neuroborreliosis can generally be diagnosed and treated successfully. Progress in microbiological research has led to improved serological tests with higher sensitivity and new approaches for early diagnosis of Lyme disease. Erythema migrans is the most frequent manifestation of Borrelia infection. It is diagnosed clinically. Neuroborreliosis is diagnosed by the combination of typical neurological symptoms, cerebrospinal fluid pleocytosis and Borrelia-specific antibodies produced intrathecally. In adults, erythema migrans is treated with doxycycline, in children with amoxicillin. Standard treatment of neuroborreliosis is ceftriaxone or cefotaxime i.v. Recent studies show similar efficacy of oral doxycycline in early neuroborreliosis. An appropriate antibiotic treatment eliminates the pathogen effectively. Repeated episodes of acute manifestations of Lyme disease in treated patients are probably due to reinfection and not to relapse. Only in a small proportion of treated patients is recovery from neuroborrelioses incomplete. In addition to neurological residual sequelae recent studies have detected persistent neuropsychological deficits in a small subgroup of patients. Conversely, when borreliosis is suspected by patients suffering from non-specific symptoms, a thorough clinical and laboratory assessment is required to identify other underlying diseases."],["dc.identifier.doi","10.1055/s-0032-1332850"],["dc.identifier.isi","000315182600002"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30782"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.relation.issn","0302-4350"],["dc.title","Update Neuroborreliosis - New and Proven Options"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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","1079"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Expert Review of Anti-infective Therapy"],["dc.bibliographiccitation.lastpage","1095"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Djukic, Marija"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Eiffert, Helmut"],["dc.date.accessioned","2018-11-07T09:19:23Z"],["dc.date.available","2018-11-07T09:19:23Z"],["dc.date.issued","2013"],["dc.description.abstract","Bacterial meningitis remains a disease with high mortality and long-term morbidity. Outcome critically depends on the rapid initiation of effective antibiotic therapy. Since a further increase of the incidence of pathogens resistant to antibacterials can be expected both in community-acquired and nosocomial bacterial meningitis, the choice of an optimum initial empirical antibiotic regimen will gain significance. In this context, the use of antibiotics which are bactericidal but do not lyse bacteria, may emerge as a therapeutic option. Conversely, the role of corticosteroids, which decrease the entry of hydrophilic antibacterials into the cerebrospinal fluid, as adjunctive therapy will probably decline as a consequence of the increasing antibiotic resistance of bacteria causing meningitis. Consequent vaccination of all children at present is the most efficient manner to reduce disease burden."],["dc.identifier.doi","10.1586/14787210.2013.839381"],["dc.identifier.isi","000325546200013"],["dc.identifier.pmid","24073921"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28620"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Taylor & Francis Ltd"],["dc.relation.issn","1744-8336"],["dc.relation.issn","1478-7210"],["dc.title","Bacterial meningitis: new therapeutic approaches"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2253"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Critical Care Medicine"],["dc.bibliographiccitation.lastpage","2258"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Lugert, Raimond"],["dc.contributor.author","Stoltefaut, Valentin"],["dc.contributor.author","Hoecht, Anna"],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2018-11-07T08:28:06Z"],["dc.date.available","2018-11-07T08:28:06Z"],["dc.date.issued","2009"],["dc.description.abstract","Objective. In bacterial meningitis, severe systemic and local inflammation causes long-term impairment and death of affected patients. The current antibiotic therapy relies on cell wall-active beta-lactam antibiotics, which rapidly sterilize the cerebrospinal fluid (CSF). However, beta-lactams inhibit cell wall synthesis, induce bacteriolysis, and thereby evoke a sudden release of high amounts of toxic and proinflammatory bacterial products. Because tissue damage in bacterial meningitis is the result of bacterial toxins and the inflammatory host response, any reduction of tree bacterial compounds promises to prevent neuronal damage. Design: In vitro experiments and randomized prospective animal study. Setting. University research laboratories. Subjects: Streptococcus pneumoniae broth cultures and New Zealand White rabbits. Interventions: We evaluated a concept to improve bacterial meningitis therapy in which a short-term pretreatment with the protein synthesis-inhibiting antibiotic rifampicin precedes the Standard antibiotic therapy with ceftriaxone. First logarithmically growing pneumococcal cultures were subdivided and exposed to different antibiotics. Then, rabbits suffering from pneumococcal meningitis were randomized to receive rifampicin pretreatment or ceftriaxone alone. Measurements and Main Results. In pneumococcal cultures, quantitative immunoblotting and real-time polymerase chain reaction revealed a reduced release of pneumolysin and bacterial DNA by rifampicin pretreatment for 30 minutes in comparison with ceftriaxone treatment alone. In vivo, a 1-hour rifampicin pretreatment reduced the release of bacterial products and attenuated the inflammatory host response, as demonstrated by decreased CSF levels of prostaglandin E2 and total protein and increased glucose CSF/plasma ratios. Rifampicin pretreatment reduced infection-associated neuronal apoptotic cell loss compared with ceftriaxone-treated controls. Conclusions. A short-term pretreatment with rifampicin reduced the beta-lactam-induced release of deleterious bacterial products, attenuated inflammation, and thereby decreased neuronal cell loss in experimental bacterial meningitis. This concept has the potential to reduce inflammation-associated neuronal injury in bacterial meningitis and should be evaluated in a clinical trial. (Crit Care Med 2009; 37:2253-2258)"],["dc.identifier.doi","10.1097/CCM.0b013e3181a036c0"],["dc.identifier.isi","000267245200018"],["dc.identifier.pmid","19487938"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6227"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16341"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0090-3493"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Short-term rifampicin pretreatment reduces inflammation and neuronal cell death in a rabbit model of bacterial meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]