Ribes, Sandra

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neuroinflammation"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Arcilla, Christa"],["dc.contributor.author","Ott, Martina"],["dc.contributor.author","Schütze, Sandra"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2020-12-10T18:39:00Z"],["dc.date.available","2020-12-10T18:39:00Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1186/s12974-020-1700-4"],["dc.identifier.eissn","1742-2094"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17124"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77507"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Pre-treatment with the viral Toll-like receptor 3 agonist poly(I:C) modulates innate immunity and protects neutropenic mice infected intracerebrally with Escherichia coli"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["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.artnumber","8"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Laboratory Animal Research"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Schütze, Sandra"],["dc.contributor.author","Manig, Anja"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2019-07-28T03:36:01Z"],["dc.date.accessioned","2021-10-27T13:21:18Z"],["dc.date.available","2019-07-28T03:36:01Z"],["dc.date.available","2021-10-27T13:21:18Z"],["dc.date.issued","2019"],["dc.date.updated","2019-07-28T03:36:01Z"],["dc.description.abstract","Geriatric animal models are crucial for a better understanding and an improved therapy of age-related diseases. We observed a high mortality of aged mice after anesthesia with a standard dose of ketamine/xylazine, an anesthetic regimen frequently used in laboratory veterinary medicine. C57BL/6-N mice at the age of 2.14 ± 0.23 months (young mice) and 26.31 ± 2.15 months (aged mice) were anesthetized by intraperitoneal injection of 2 mg ketamine and 0.2 mg xylazine. 4 of 26 aged mice (15.4%) but none of 26 young mice died within 15 min after injection of the anesthetics. The weight of aged mice was significantly higher than that of young mice (32.8 ± 5.4 g versus 23.2 ± 3.4 g, p < 0.0001). Thus, aged mice received lower doses of anesthetics in relation to their body weight which are within the lower range of doses recommended in the literature or even beneath. There were no differences between deceased and surviving aged mice concerning their sex, weight and their motor performance prior to anesthesia. Our data clearly show an age-related increase of mortality upon anesthesia with low standard doses of ketamine/xylazine. Assessment of weight and motor performance did not help to predict vulnerability of aged mice to the anesthetics. Caution is necessary when this common anesthetic regimen is applied in aged mice: lower doses or the use of alternative anesthetics should be considered to avoid unexpected mortality. The present data from our geriatric mouse model strongly corroborate an age-adjusted reduction of anesthetic doses to reduce anesthesia-related mortality in aged individuals."],["dc.identifier.doi","10.1186/s42826-019-0008-y"],["dc.identifier.pmid","32257896"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16309"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92010"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 4.0"],["dc.rights.holder","The Author(s)"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Aged mice show an increased mortality after anesthesia with a standard dose of ketamine/xylazine"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["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.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"]]