Wellmer, Andreas

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

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

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

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

[["dc.bibliographiccitation.firstpage","490"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","European Journal of Clinical Microbiology & Infectious Diseases"],["dc.bibliographiccitation.lastpage","493"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Fleischer, H."],["dc.contributor.author","Wellmer, A."],["dc.contributor.author","Munzel, U."],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T08:54:47Z"],["dc.date.available","2018-11-07T08:54:47Z"],["dc.date.issued","2001"],["dc.description.abstract","In order to study the release of DNA from Streptococcus pneumoniae in vitro during spontaneous growth and treatment with ceftriaxone or rifampin, a semiquantitative polymerase chain reaction was used. During spontaneous growth, high concentrations of bacterial DNA were released. Exposure to 10 mug/ml of ceftriaxone decreased the DNA release, in median, by 19 times (P=0.03 vs. spontaneous growth). Treatment with 10 mug/ml of rifampin led to a reduction of DNA release, in median, by a factor of 49 (P=0.03 vs. ceftriaxone; six experiments performed on different days)."],["dc.identifier.isi","000170686200008"],["dc.identifier.pmid","11561806"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22749"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0934-9723"],["dc.title","Reduced release of DNA from Streptococcus pneumoniae after treatment with rifampin in comparison to spontaneous growth and ceftriaxone treatment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","6504"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Infection and Immunity"],["dc.bibliographiccitation.lastpage","6508"],["dc.bibliographiccitation.volume","70"],["dc.contributor.author","Wellmer, A."],["dc.contributor.author","Zysk, G."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Kunst, T."],["dc.contributor.author","von Mering, M."],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T09:52:27Z"],["dc.date.available","2018-11-07T09:52:27Z"],["dc.date.issued","2002"],["dc.description.abstract","Pneumolysin, neuraminidases A and B, and hyaluronidase are virulence factors of Streptococcus pneumoniae that appear to be involved in the pathogenesis of meningitis. In a murine model of meningitis after intracerebral infection using mutants of S. pneumoniae D39, only mice infected with a pneumolysin-deficient strain were healthier at 32 and 36 h, had lower bacterial titers in blood at 36 h, and survived longer than the D39 parent strain. Cerebellar and spleen bacterial titers, meningeal inflammation, and neuronal damage scores remained uninfluenced by the lack of any of the virulence factors."],["dc.identifier.doi","10.1128/IAI.70.11.6504-6508.2002"],["dc.identifier.isi","000178675100075"],["dc.identifier.pmid","12379738"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36126"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Microbiology"],["dc.relation.issn","0019-9567"],["dc.title","Decreased virulence of a pneumolysin-deficient strain of Streptococcus pneumoniae in murine meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]