Nau, Roland

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","131"],["dc.bibliographiccitation.journal","BMC infectious diseases"],["dc.bibliographiccitation.lastpage","12"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Goos, Miriam"],["dc.contributor.author","Zech, Wolf-Dieter"],["dc.contributor.author","Jaiswal, Manoj Kumar"],["dc.contributor.author","Balakrishnan, Saju"],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Mitchell, Timothy"],["dc.contributor.author","Carrì, Maria Teresa"],["dc.contributor.author","Keller, Bernhard U."],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2019-07-10T08:13:02Z"],["dc.date.available","2019-07-10T08:13:02Z"],["dc.date.issued","2007"],["dc.description.abstract","Background: Infections can aggravate the course of neurodegenerative diseases including amyotrophic lateral sclerosis (ALS). Mutations in the anti-oxidant enzyme Cu,Zn superoxide dismutase (EC 1.15.1.1, SOD1) are associated with familial ALS. Streptococcus pneumoniae, the most frequent respiratory pathogen, causes damage by the action of the cholesterol-binding virulence factor pneumolysin and by stimulation of the innate immune system, particularly via Toll-like-receptor 2. Methods: SH-SY5Y neuroblastoma cells transfected with the G93A mutant of SOD1 typical for familial ALS (G93A-SOD1) and SH-SY5Y neuroblastoma cells ...Results: SH-SY5Y neuroblastoma cells transfected with the G93A mutant of SOD1 typical for familial ALS (G93A-SOD1) were more vulnerable to the neurotoxic action of pneumolysin and to the attack of monocytes stimulated by Pam3CSK4 than SH-SY5Y cells transfected with wild-type human SOD1. The enhanced pneumolysin toxicity in G93A-SOD1 neuronal cells depended on the inability of these cells to cope with an increased calcium influx caused by pores formed by pneumolysin ...Conclusion: The particular vulnerability of G93A-SOD1 neuronal cells to hemolysins and inflammation may be partly responsible for the clinical deterioration of ALS patients during infections. These findings link infection and motor neuron disease and suggest early treatment of respiratory infections in ALS patients."],["dc.identifier.fs","194629"],["dc.identifier.ppn","559657781"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/4376"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/61105"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","616"],["dc.title","Expression of a Cu,Zn superoxide dismutase typical for familial amyotrophic lateral sclerosis increases the vulnerability of neuroblastoma cells to infectious injury"],["dc.title.alternative","Research article"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","557"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Infection and Immunity"],["dc.bibliographiccitation.lastpage","564"],["dc.bibliographiccitation.volume","77"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Czesnik, Dirk"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Zeug, Andre"],["dc.contributor.author","Bukowski, Stephanie"],["dc.contributor.author","Mildner, Alexander"],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Hammerschmidt, Sven"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2018-11-07T08:34:37Z"],["dc.date.available","2018-11-07T08:34:37Z"],["dc.date.issued","2009"],["dc.description.abstract","Meningitis and meningoencephalitis caused by Escherichia coli are associated with high rates of mortality. When an infection occurs, Toll-like receptors (TLRs) expressed by microglial cells can recognize pathogen-associated molecular patterns and activate multiple steps in the inflammatory response that coordinate the brain's local defense, such as phagocytosis of invading pathogens. An upregulation of the phagocytic ability of reactive microglia could improve the host defense in immunocompromised patients against pathogens such as E. coli. Here, murine microglial cultures were stimulated with the TLR agonists Pam(3)CSK(4) (TLR1/TLR2), lipopolysaccharide (TLR4), and CpG oligodeoxynucleotide (TLR9) for 24 h. Upon stimulation, levels of tumor necrosis factor alpha and the neutrophil chemoattractant CXCL1 were increased, indicating microglial activation. Phagocytic activity was studied after adding either E. coli DH5 alpha or E. coli K1 strains. After 60 and 90 min of bacterial exposure, the number of ingested bacteria was significantly higher in cells prestimulated with TLR agonists than in unstimulated controls (P < 0.01). Addition of cytochalasin D, an inhibitor of actin polymerization, blocked >90% of phagocytosis. We also analyzed the ability of microglia to kill the ingested E. coli strains. Intracellularly surviving bacteria were quantified at different time points (90, 150, 240, and 360 min) after 90 min of phagocytosis. The number of bacteria killed intracellularly after 6 h was higher in cells primed with the different TLR agonists than in unstimulated microglia. Our data suggest that microglial stimulation by the TLR system can increase bacterial phagocytosis and killing. This approach could improve central nervous system resistance to infections in immunocompromised patients."],["dc.identifier.doi","10.1128/IAI.00903-08"],["dc.identifier.isi","000262776100058"],["dc.identifier.pmid","18981243"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7765"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17860"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Microbiology"],["dc.relation.issn","0019-9567"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Toll-Like Receptor Prestimulation Increases Phagocytosis of Escherichia coli DH5 alpha and Escherichia coli K1 Strains by Murine Microglial Cells"],["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"]]