Bunkowski, Stephanie

[["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.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.volume","228"],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Loleit, Tobias"],["dc.contributor.author","Zeretzke, Moritz"],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2018-11-07T08:36:51Z"],["dc.date.available","2018-11-07T08:36:51Z"],["dc.date.issued","2010"],["dc.identifier.isi","000283694400048"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18406"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","10th Congress of the International-Society-of-Neuroimmunology (ISNI)"],["dc.relation.eventlocation","Sitges, SPAIN"],["dc.title","Additive microglial-mediated neuronal injury induced by Amyloid-beta and bacterial TLR agonists"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","367"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","376"],["dc.bibliographiccitation.volume","58"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Czesnik, Dirk"],["dc.contributor.author","Scheffel, Joerg"],["dc.contributor.author","Zeug, Andre"],["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","2018-11-07T08:46:15Z"],["dc.date.available","2018-11-07T08:46:15Z"],["dc.date.issued","2010"],["dc.description.abstract","Microglia express Toll-like receptors (TLRs) that recognize invading pathogens as well as endogenous proteins such as fibronectin under nonphysiological conditions. Here, we demonstrated that fibronectin stimulates murine microglia in culture in a dose-dependent manner: microglial cells secreted proinflammatory cytokines and chemokines and increased phagocytosis of Escherichia coli DH5 alpha and E. coli K1 strains. Low levels of fibronectin exerted a synergistic effect on the release of proinflammatory compounds by microglia co-stimulated with agonists for TLR1/2 (Pam(3)CSK(4)) or TLR9 (CpG DNA), but not in combination with the TLR4 agonist lipopolysaccharide (LPS). Phagocytosis of bacterial strains was moderately enhanced when microglia was co-stimulated with high concentrations of fibronectin and one pathogen-derived TLR agonist. In conclusion, fibronectin increased proinflammatory and phagocytotic functions in microglia and partially synergized with microbial TLR agonists. (C) 2009 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/glia.20929"],["dc.identifier.isi","000273189600009"],["dc.identifier.pmid","19780198"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20644"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0894-1491"],["dc.title","Fibronectin Stimulates Escherichia coli Phagocytosis by Microglial Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","12573"],["dc.bibliographiccitation.issue","24"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","12592"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Schütze, Sandra"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Kaufmann, Annika"],["dc.contributor.author","Manig, Anja"],["dc.contributor.author","Scheffel, Jörg"],["dc.contributor.author","Redlich, Sandra"],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2019-07-10T08:11:52Z"],["dc.date.available","2019-07-10T08:11:52Z"],["dc.date.issued","2014-12-30"],["dc.description.abstract","Incidence and mortality of bacterial meningitis are strongly increased in aged compared to younger adults demanding new strategies to improve prevention and therapy of bacterial central nervous system (CNS) infections the elderly. Here, we established a geriatric mouse model for an intracerebral E. coli infection which reflects the clinical situation in aged patients: After intracerebral challenge with E. coli K1, aged mice showed a higher mortality, a faster development of clinical symptoms, and a more pronounced weight loss. Elimination of bacteria and systemic inflammatory response were impaired in aged mice, however, the number of infiltrating leukocytes and microglial cells in the CNS of aged and young mice did not differ substantially. In vitro, primary microglial cells and peritoneal macrophages from aged mice phagocytosed less E. coli and released less NO and cyto-/chemokines compared to cells from young mice both without activation and after stimulation by agonists of TLR 2, 4, and 9. Our results suggest that the age-related decline of microglia and macrophage functions plays an essential role for the higher susceptibility of aged mice to intracerebral infections. Strategies to improve the phagocytic potential of aged microglial cells and macrophages appear promising for prevention and treatment of CNS infections in elderly patients."],["dc.identifier.fs","611430"],["dc.identifier.pmid","25528768"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11618"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60812"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1949-2553"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 3.0"],["dc.rights.uri","http://creativecommons.org/licenses/by/3.0"],["dc.title","Higher mortality and impaired elimination of bacteria in aged mice after intracerebral infection with E. coli are associated with an age-related decline of microglia and macrophage functions."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","748"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Neuropathology and Experimental Neurology"],["dc.bibliographiccitation.lastpage","757"],["dc.bibliographiccitation.volume","70"],["dc.contributor.author","Tauber, Simone C."],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Heinz, Torsten"],["dc.contributor.author","Fingerle, Volker"],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Kugelstadt, Dominik"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Jahn, Olaf"],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2018-11-07T08:52:48Z"],["dc.date.available","2018-11-07T08:52:48Z"],["dc.date.issued","2011"],["dc.description.abstract","Lyme neuroborreliosis (LNB) is the most frequent tick-borne infectious disease of the central nervous system. In acute LNB and the rare chronic state of infection, patients can experience cognitive deficits such as attention and memory disturbances. During LNB, single compounds of Borrelia burgdorferi sensu lato are released into the subarachnoid space. To investigate the pathogenesis of neurologic dysfunction in LNB, we determined that the outer surface protein C (OspC), a major virulence factor of B. burgdorferi, stimulated mouse microglial cells in a dose-dependent manner to release nitric oxide (EC(50) = 0.24 mg/L) in vitro. To mimic pathophysiologic conditions of long-term release of this bacterial component in vivo, we treated C57BL/6 mice with recombinant OspC from Borrelia garinii or buffer by intraventricular infusion and tested them for behavioral deficits. After 4 weeks, brains were examined by routine histology and immunohistochemistry. Assessment of spatial learning and memory of treated mice during OspC exposure did not reveal significant differences from controls. Continuous exposure to intrathecal B. burgdorferi OspC led to activation of microglia and axonal damage without demonstrable cognitive impairment in experimental mice. These results suggest that long-term intrathecal exposure to OspC resulted in axonal damage that may underlie the neurologic manifestations in chronic LNB."],["dc.description.sponsorship","Else Kroner-Fresenius-Stiftung, Bad Homburg v.d.H., Germany"],["dc.identifier.doi","10.1097/NEN.0b013e3182289acd"],["dc.identifier.isi","000294247700002"],["dc.identifier.pmid","21865883"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22260"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0022-3069"],["dc.title","Long- Term Intrathecal Infusion of Outer Surface Protein C From Borrelia burgdorferi Causes Axonal Damage"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","17"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neuroscience Letters"],["dc.bibliographiccitation.lastpage","20"],["dc.bibliographiccitation.volume","482"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Adam, Nina"],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2018-11-07T08:39:07Z"],["dc.date.available","2018-11-07T08:39:07Z"],["dc.date.issued","2010"],["dc.description.abstract","Stimulation of murine primary microglia with Toll-like receptor (TLR) agonists enhances their ability to phagocytose and kill bacteria. Here we show that the viral TLR3 agonist poly(I:C) stimulates the release of cyto-/chemokines and nitric oxide by microglia. Poly(I:C) increases microglial phagocytosis and intracellular killing of Escherichia coli K1, a pathogenic encapsulated bacterial strain, after 30 and 90 min of co-incubation. Stimulation with a viral epitope may strengthen the resistance of the brain to bacterial infections in vivo. Our data encourage animal experiments with poly(LC) derivatives to assess whether this approach can increase the resistance of the CNS against bacterial infections. (C) 2010 Elsevier Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.neulet.2010.06.078"],["dc.identifier.isi","000281274000004"],["dc.identifier.pmid","20599470"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18916"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Ireland Ltd"],["dc.relation.issn","0304-3940"],["dc.title","The viral TLR3 agonist poly(I:C) stimulates phagocytosis and intracellular killing of Escherichia coli by microglial cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Zeitschrift für Gerontologie und Geriatrie"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Manig, Anja"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Nau, R."],["dc.contributor.author","Schuetze, Sandra"],["dc.date.accessioned","2018-11-07T09:52:36Z"],["dc.date.available","2018-11-07T09:52:36Z"],["dc.date.issued","2015"],["dc.format.extent","51"],["dc.identifier.isi","000360847800161"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36160"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","1435-1269"],["dc.relation.issn","0948-6704"],["dc.title","Process of Streptococcus pneumoniae -Meningitis in the old and young Mice"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","20"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Immunity & Ageing"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Manig, Anja"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Diesselberg, Catharina"],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Schütze, Sandra"],["dc.date.accessioned","2019-07-09T11:45:50Z"],["dc.date.available","2019-07-09T11:45:50Z"],["dc.date.issued","2018"],["dc.description.abstract","Abstract In order to elucidate the causes for the increased mortality of aged patients with bacterial central nervous system (CNS) infections, we compared the course of Streptococcus pneumoniae (S. pneumoniae) meningitis in aged and young mice. Aged (21.2 ± 3.1 months, n = 40) and young (3.2 ± 0.9 months, n = 42) C57BL/6N and B6/SJL mice were infected by intracerebral injection of 50–70 CFU S. pneumoniae serotype 3 and monitored for 15 days. Aged and young mice did not differ concerning mortality (35% versus 38%), weight loss, development of clinical symptoms, bacterial concentrations in cerebellum and spleen as well as the number of leukocytes infiltrating the CNS. In contrast to results from our geriatric mouse model of Escherichia coli (E. coli) meningitis, where aged mice showed a higher mortality and an impaired elimination of bacteria, we did not find any differences between aged and young mice after intracerebral infection with S. pneumoniae serotype 3. This indicates that the increased susceptibility of aged mice to bacterial CNS infections is pathogen-specific: It appears less prominent in infections caused by hardly phagocytable pathogens with thick capsules like S. pneumoniae serotype 3, where the age-related decline of the phagocytic capacity of microglia and macrophages has a minor influence on the disease course."],["dc.identifier.doi","10.1186/s12979-018-0129-4"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15325"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59318"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.publisher","BioMed Central"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Age does not influence the disease course in a mouse model of Streptococcus pneumoniae serotype 3 meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","651"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Alzheimer s Disease"],["dc.bibliographiccitation.lastpage","657"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Schuetze (nee Ebert), Sandra"],["dc.contributor.author","Loleit, Tobias"],["dc.contributor.author","Zeretzke, Moritz"],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2018-11-07T09:15:00Z"],["dc.date.available","2018-11-07T09:15:00Z"],["dc.date.issued","2012"],["dc.description.abstract","Activated microglia is considered to be involved in the progression of Alzheimer's disease (AD). We investigated the effect of amyloid-beta(1-40) (A beta(40)) and exogenous agonists of Toll-like receptor (TLR) 1/2 (Pam(3)CSK(4)) and TLR4 (LPS) on neurons in primary murine neuron-microglia co-cultures. Neuronal viability, assessed by quantifying the number of intact neuronal extensions and their crossings using a newly developed Definiens Cognition Network Technology-based method, was significantly decreased after treatment with Pam(3)CSK(4), LPS, and A beta(40). Combined treatment with A beta(40) and Pam(3)CSK(4) or LPS had an additive effect. Hence, in patients with AD, synergistic microglial activation by A beta and bacterial products during infections might contribute to disease progression."],["dc.identifier.doi","10.3233/JAD-2012-120856"],["dc.identifier.isi","000308197000017"],["dc.identifier.pmid","22647259"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27567"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Ios Press"],["dc.relation.issn","1387-2877"],["dc.title","Additive Microglia-Mediated Neuronal Injury Caused by Amyloid-beta and Bacterial TLR Agonists in Murine Neuron-Microglia Co-Cultures Quantified by an Automated Image Analysis using Cognition Network Technology"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","175"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neuroinflammation"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Diesselberg, Catharina"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Seele, Jana"],["dc.contributor.author","Kaufmann, Annika"],["dc.contributor.author","Redlich, Sandra"],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Schütze, Sandra"],["dc.date.accessioned","2019-07-09T11:45:31Z"],["dc.date.available","2019-07-09T11:45:31Z"],["dc.date.issued","2018"],["dc.description.abstract","BACKGROUND: Bacterial meningitis is associated with high mortality and long-term neurological sequelae. Increasing the phagocytic activity of microglia could improve the resistance of the CNS against infections. We studied the influence of activin A, a member of the TGF-β family with known immunoregulatory and neuroprotective effects, on the functions of microglial cells in vitro. METHODS: Primary murine microglial cells were treated with activin A (0.13 ng/ml-13 μg/ml) alone or in combination with agonists of TLR2, 4, and 9. Phagocytosis of Escherichia coli K1 as well as release of TNF-α, IL-6, CXCL1, and NO was assessed. RESULTS: Activin A dose-dependently enhanced the phagocytosis of Escherichia coli K1 by microglial cells activated by agonists of TLR2, 4, and 9 without further increasing NO and proinflammatory cytokine release. Cell viability of microglial cells was not affected by activin A. CONCLUSIONS: Priming of microglial cells with activin A could increase the elimination of bacteria in bacterial CNS infections. This preventive strategy could improve the resistance of the brain to infections, particularly in elderly and immunocompromised patients."],["dc.identifier.doi","10.1186/s12974-018-1209-2"],["dc.identifier.pmid","29880000"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15236"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59248"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","BioMed Central"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Activin A increases phagocytosis of Escherichia coli K1 by primary murine microglial cells activated by toll-like receptor agonists"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]