Ribes, Sandra

[["dc.bibliographiccitation.artnumber","108"],["dc.bibliographiccitation.journal","Journal of Neuroinflammation"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Redlich, Sandra"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Schutze, Sandra"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2018-11-07T09:38:56Z"],["dc.date.available","2018-11-07T09:38:56Z"],["dc.date.issued","2014"],["dc.description.abstract","Background: Palmitoylethanolamide (PEA), an endogenous lipid and a congener of anandamide, possesses a wide range of effects related to metabolic and cellular homeostasis including anti-inflammatory and neuroprotective properties. Methods: In vitro, we studied the ability of macrophages to phagocytose Escherichia coli K1 after stimulation with increasing doses of PEA. In vivo, wild-type mice were treated with PEA intraperitoneally 12 hours and 30 minutes before infection. Meningoencephalitis or sepsis was induced by intracerebral or intraperitoneal infection with E. coli K1. Results: Stimulation of macrophages with PEA for 30 minutes increased the phagocytosis of E. coli K1 without inducing the release of TNF alpha or CXCL1. Intracellular killing of E. coli K1 was higher in PEA-stimulated than in unstimulated peritoneal macrophages and microglial cells. Pre-treatment with PEA significantly increased survival of mice challenged intracerebrally or intraperitoneally with E. coli K1. This effect was associated with a decreased production of CXCL1, IL-1 beta and IL-6 in homogenates of spleen and cerebellum in mice treated with PEA. Conclusions: Our observations suggest that these protective effects of PEA in mice can increase the resistance to bacterial infections without the hazard of collateral damage by excessive stimulation of phagocytes."],["dc.identifier.doi","10.1186/1742-2094-11-108"],["dc.identifier.isi","000338670800001"],["dc.identifier.pmid","24927796"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10430"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33166"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1742-2094"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Palmitoylethanolamide stimulates phagocytosis of Escherichia coli K1 by macrophages and increases the resistance of mice against infections"],["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.artnumber","39"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neuroinflammation"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Ribes, S."],["dc.contributor.author","Zacke, L."],["dc.contributor.author","Nessler, S."],["dc.contributor.author","Saiepour, N."],["dc.contributor.author","Avendaño-Guzmán, E."],["dc.contributor.author","Ballüer, M."],["dc.contributor.author","Hanisch, U. K."],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2021-04-14T08:28:08Z"],["dc.date.accessioned","2022-08-16T13:10:55Z"],["dc.date.available","2021-04-14T08:28:08Z"],["dc.date.available","2022-08-16T13:10:55Z"],["dc.date.issued","2021-02-02"],["dc.date.updated","2022-07-29T12:17:30Z"],["dc.description.abstract","Background\r\n Bacterial meningitis is a fatal disease with a mortality up to 30% and neurological sequelae in one fourth of survivors. Available vaccines do not fully protect against this lethal disease. Here, we report the protective effect of synthetic oligodeoxynucleotides containing unmethylated cytosine-guanine motifs (CpG ODN) against the most frequent form of bacterial meningitis caused by Streptococcus pneumoniae.\r\n \r\n \r\n Methods\r\n Three days prior to the induction of meningitis by intracerebral injection of S. pneumoniae D39, wild-type and Toll-like receptor (TLR9)−/− mice received an intraperitoneal injection of 100 μg CpG ODN or vehicle. To render mice neutropenic, anti-Ly-6G monoclonal antibody was daily administrated starting 4 days before infection with a total of 7 injections. Kaplan-Meier survival analyses and bacteriological studies, in which mice were sacrificed 24 h and 36 h after infection, were performed.\r\n \r\n \r\n Results\r\n Pre-treatment with 100 μg CpG ODN prolonged survival of immunocompetent and neutropenic wild-type mice but not of TLR9−/− mice. There was a trend towards lower mortality in CpG ODN-treated immunocompetent and neutropenic wild-type mice. CpG ODN caused an increase of IL-12/IL-23p40 levels in the spleen and serum in uninfected animals. The effects of CpG ODN on bacterial concentrations and development of clinical symptoms were associated with an increased number of microglia in the CNS during the early phase of infection. Elevated concentrations of IL-12/IL-23p40 and MIP-1α correlated with lower bacterial concentrations in the blood and spleen during infection.\r\n \r\n \r\n Conclusions\r\n Pre-conditioning with CpG ODN strengthened the resistance of neutropenic and immunocompetent mice against S. pneumoniae meningitis in the presence of TLR9. Administration of CpG ODN decreased bacterial burden in the cerebellum and reduced the degree of bacteremia. Systemic administration of CpG ODN may help to prevent or slow the progression to sepsis of bacterial CNS infections in healthy and immunocompromised individuals even after direct inoculation of bacteria into the intracranial compartments, which can occur after sinusitis, mastoiditis, open head trauma, and surgery, including placement of an external ventricular drain."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.citation","Journal of Neuroinflammation. 2021 Feb 02;18(1):39"],["dc.identifier.doi","10.1186/s12974-021-02077-3"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17725"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82510"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112768"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","1742-2094"],["dc.relation.orgunit","Institut für Neuropathologie"],["dc.rights","CC BY 4.0"],["dc.rights.holder","The Author(s)"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject","Oligodeoxynucleotides containing unmethylated cytosine-guanine motifs (CpG ODN)"],["dc.subject","Streptococcus pneumoniae"],["dc.subject","Meningitis"],["dc.subject","Toll-like receptor (TLR) 9"],["dc.subject","Interleukin (IL)-12/IL-23p40"],["dc.subject","Microglia"],["dc.subject","Macrophage inflammatory protein (MIP)-1α"],["dc.title","Oligodeoxynucleotides containing unmethylated cytosine-guanine motifs are effective immunostimulants against pneumococcal meningitis in the immunocompetent and neutropenic host"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1083"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","1099"],["dc.bibliographiccitation.volume","63"],["dc.contributor.author","Menzfeld, Christiane"],["dc.contributor.author","John, Michael"],["dc.contributor.author","van Rossum, Denise"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Scheffel, Joerg"],["dc.contributor.author","Janova, Hana"],["dc.contributor.author","Goetz, Alexander A."],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Borisch, Angela"],["dc.contributor.author","Boutin, Philippe"],["dc.contributor.author","Neumann, Konstantin"],["dc.contributor.author","Bremes, Vanessa"],["dc.contributor.author","Wienands, Juergen"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Tischner, Denise"],["dc.contributor.author","Waetzig, Vicky"],["dc.contributor.author","Herdegen, Thomas"],["dc.contributor.author","Teismann, Peter"],["dc.contributor.author","Greig, Iain"],["dc.contributor.author","Mueller, Michael"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Mildner, Alexander"],["dc.contributor.author","Kettenmann, Helmut"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Prinz, Marco R."],["dc.contributor.author","Rotshenker, Shlomo"],["dc.contributor.author","Weber, Martin S."],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.date.accessioned","2018-11-07T09:56:53Z"],["dc.date.available","2018-11-07T09:56:53Z"],["dc.date.issued","2015"],["dc.description.abstract","The putative protein tyrosine kinase (PTK) inhibitor tyrphostin AG126 has proven beneficial in various models of inflammatory disease. Yet molecular targets and cellular mechanisms remained enigmatic. We demonstrate here that AG126 treatment has beneficial effects in experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis. AG126 alleviates the clinical symptoms, diminishes encephalitogenic Th17 differentiation, reduces inflammatory CNS infiltration as well as microglia activation and attenuates myelin damage. We show that AG126 directly inhibits Bruton's tyrosine kinase (BTK), a PTK associated with B cell receptor and Toll-like receptor (TLR) signaling. However, BTK inhibition cannot account for the entire activity spectrum. Effects on TLR-induced proinflammatory cytokine expression in microglia involve AG126 hydrolysis and conversion of its dinitrile side chain to malononitrile (MN). Notably, while liberated MN can subsequently mediate critical AG126 features, full protection in EAE still requires delivery of intact AG126. Its anti-inflammatory potential and especially interference with TLR signaling thus rely on a dual mechanism encompassing BTK and a novel MN-sensitive target. Both principles bear great potential for the therapeutic management of disturbed innate and adaptive immune functions. GLIA 2015;63:1083-1099"],["dc.identifier.doi","10.1002/glia.22803"],["dc.identifier.isi","000353244400011"],["dc.identifier.pmid","25731696"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37056"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.title","Tyrphostin AG126 Exerts Neuroprotection in CNS Inflammation by a Dual Mechanism"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","14"],["dc.bibliographiccitation.journal","Journal of Neuroinflammation"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Meister, Tanja"],["dc.contributor.author","Ott, Martina"],["dc.contributor.author","Redlich, Sandra"],["dc.contributor.author","Janova, Hana"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2018-11-07T09:45:02Z"],["dc.date.available","2018-11-07T09:45:02Z"],["dc.date.issued","2014"],["dc.description.abstract","Background: Prophylaxis with unmethylated cytosine phosphate guanidine (CpG) oligodeoxynucleotides (ODN) protects against several systemic experimental infections. Escherichia coli is a major cause of Gram-negative neonatal bacterial meningitis and also causes meningitis and meningoencephalitis in older and immunocompromised patients. Methods: Wild-type (wt) and Toll-like receptor 9 (TLR9)-deficient mice were rendered neutropenic by intraperitoneal administration of the anti-Ly-6G monoclonal antibody. Immunocompetent and neutropenic mice received intraperitoneal CpG ODN or vehicle 72 h prior to induction of E. coli K1 meningoencephalitis. Results: Pre-treatment with CpG ODN significantly increased survival of neutropenic wt mice from 33% to 75% (P = 0.0003) but did not protect neutropenic TLR9(-/-) mice. The protective effect of CpG ODN was associated with an enhanced production of interleukin (IL)-12/IL-23p40 with sustained increased levels in serum and spleen at least for 17 days after conditioning compared to buffer-treated animals. CpG-treated neutropenic wt mice showed reduced bacterial concentrations and increased recruitment of Ly6C(high)CCR2(+) monocytes in brain and spleen 42 h after infection. The levels of macrophage inflammatory protein 1 alpha (MIP-1 alpha) and interferon gamma (IFN-gamma) in spleen were higher 42 h after infection in CpG-treated compared to buffer-treated neutropenic animals. In immunocompetent mice, prophylaxis with CpG ODN did not significantly increase survival compared to the buffer group (60% vs. 45%, P = 0.2). Conclusions: These findings suggest that systemic administration of CpG ODN may help to prevent bacterial CNS infections in immunocompromised individuals."],["dc.identifier.doi","10.1186/1742-2094-11-14"],["dc.identifier.isi","000333212600001"],["dc.identifier.pmid","24456653"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9757"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34526"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1742-2094"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Intraperitoneal prophylaxis with CpG oligodeoxynucleotides protects neutropenic mice against intracerebral Escherichia coli K1 infection"],["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.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","615"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Shock"],["dc.bibliographiccitation.lastpage","619"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Diesselberg, Catharina"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Redlich, Sandra"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Schuetze, Sandra"],["dc.date.accessioned","2018-11-07T09:03:01Z"],["dc.date.available","2018-11-07T09:03:01Z"],["dc.date.issued","2012"],["dc.description.abstract","Follistatin (FS) is the binding protein of activin A and inhibits its actions. The activin/FS system participates in the fine tuning of the immune response, and concentrations of activin A and FS are elevated in serum of patients with sepsis. Intraperitoneal injection of FS markedly reduced mortality after lipopolysaccharide-induced inflammation in a mouse model. Here, we investigated whether FS also influences the disease course in a mouse model of sepsis induced by intraperitoneal injection of Escherichia coli K1, a gram-negative bacterium frequently causing septic bacterial infections. Intraperitoneal injection of 10 mu g/mL FS 30 min before infection did not influence survival, weight, motor performance, or bacterial titers of the infected mice. Thus, we could not confirm the protective effect of FS observed during lipopolysaccharide-induced inflammation in our mouse model of E. coli sepsis. Although it is a promising therapeutic tool in chronic or acute inflammatory conditions not caused by virulent pathogens, FS does not seem to increase the resistance to bacterial infections."],["dc.identifier.doi","10.1097/SHK.0b013e3182748d96"],["dc.identifier.isi","000311338900007"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24807"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1540-0514"],["dc.relation.issn","1073-2322"],["dc.title","FOLLISTATIN DOES NOT INFLUENCE THE COURSE OF ESCHERICHIA COLI K1 SEPSIS IN A MOUSE MODEL"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.volume","61"],["dc.contributor.author","Janova, Hana"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","van Rossum, Denise"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Goetz, Alexander A."],["dc.contributor.author","Nau, R."],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Hanisch, U-K"],["dc.date.accessioned","2018-11-07T09:23:23Z"],["dc.date.available","2018-11-07T09:23:23Z"],["dc.date.issued","2013"],["dc.format.extent","S181"],["dc.identifier.isi","000320408400581"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29563"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.conference","11th European Meeting on Glial Cell Function in Health and Disease"],["dc.relation.eventlocation","Berlin, GERMANY"],["dc.relation.issn","0894-1491"],["dc.title","CD14 AS A KEY REGULATOR OF TLR-MEDIATED RESPONSES OF MICROGLIA"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","150"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","The Journal of Infectious Diseases"],["dc.bibliographiccitation.lastpage","158"],["dc.bibliographiccitation.volume","215"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Heide, Ev-Christin"],["dc.contributor.author","Malzahn, Dörthe"],["dc.contributor.author","Perske, Christina"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2018-11-07T10:28:48Z"],["dc.date.available","2018-11-07T10:28:48Z"],["dc.date.issued","2017"],["dc.description.abstract","Background. The adaptive immune system has been considered to play a minimal role in the early host response during bacterial meningitis. Methods. We investigated the progression and outcome of pneumococcal meningitis in Rag1(-/-) mice lacking functional B and T cells by assessing overall and symptom-free survival, bacteriological and histological studies, as well as flow cytometry and measurements of proinflammatory mediators. Results. The intracerebral injection of S. pneumoniae D39 induced the recruitment of B and T cells (CD4+, gamma delta and natural killer) into the brain of wild-type mice. Mice with no functional B and T cells developed clinical symptoms and succumbed to the infection earlier than the wild-type group. In the CNS, Rag1(-/-) mice showed lower levels of interleukin 1 beta, reduced microglial proliferation, and impaired granulocyte recruitment with an earlier spread of pneumococci into the bloodstream, compared with wild-type mice. Lack of B and T cells resulted in a severe impairment of bacterial clearance in blood, spleen, and liver and an exaggerated systemic inflammatory response. Conclusions. B and T cells are important effector cells delaying the spread of pneumococci from the brain to the systemic circulation and shaping the immune response, thereby prolonging the survival of the host in the absence of antibiotic treatment."],["dc.identifier.doi","10.1093/infdis/jiw517"],["dc.identifier.isi","000397203500022"],["dc.identifier.pmid","27803171"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43504"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1537-6613"],["dc.relation.issn","0022-1899"],["dc.title","The Early Adaptive Immune Response in the Pathophysiological Process of Pneumococcal Meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1930"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","1943"],["dc.bibliographiccitation.volume","60"],["dc.contributor.author","Scheffel, Joerg"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","van Rossum, Denise"],["dc.contributor.author","Seifert, Stefanie"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Parsa, Roham"],["dc.contributor.author","Harris, Robert A."],["dc.contributor.author","Boddeke, Hendrikus W. G. M."],["dc.contributor.author","Chuang, Han-Ning"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Wessels, Johannes Theodor"],["dc.contributor.author","Juergens, Tanja"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Schnaars, Mareike"],["dc.contributor.author","Simons, Mikael"],["dc.contributor.author","Kettenmann, Helmut"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.date.accessioned","2018-11-07T09:03:06Z"],["dc.date.available","2018-11-07T09:03:06Z"],["dc.date.issued","2012"],["dc.description.abstract","The sentinel and immune functions of microglia require rapid and appropriate reactions to infection and damage. Their Toll-like receptors (TLRs) sense both as threats. However, whether activated microglia mount uniform responses or whether subsets conduct selective tasks is unknown. We demonstrate that murine microglia reorganize their responses to TLR activations postnatally and that this process comes with a maturation of TLR4-organized functions. Although induction of MHCI for antigen presentation remains as a pan-populational feature, synthesis of TNFa becomes restricted to a subset, even within adult central nervous system regions. Response heterogeneity is evident ex vivo, in situ, and in vivo, but is not limited to TNFa production or to TLR-triggered functions. Also, clearance activities for myelin under physiological and pathophysiological conditions, IFN >> factors reveal dissimilar microglial contributions. Notably, response heterogeneity is also confirmed in human brain tissue. Our findings suggest that microglia divide by constitutive and inducible capacities. Privileged production of inflammatory mediators assigns a master control to subsets. Sequestration of clearance of endogenous material versus antigen presentation in exclusive compartments can separate potentially interfering functions. Finally, subsets rather than a uniform population of microglia may assemble the reactive phenotypes in responses during infection, injury, and rebuilding, warranting consideration in experimental manipulation and therapeutic strategies. (c) 2012 Wiley Periodicals, Inc."],["dc.identifier.doi","10.1002/glia.22409"],["dc.identifier.isi","000310262600010"],["dc.identifier.pmid","22911652"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24833"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0894-1491"],["dc.title","Toll-like receptor activation reveals developmental reorganization and unmasks responder subsets of microglia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]