Saiepour, Nasrin

[["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","E400"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","E401"],["dc.bibliographiccitation.volume","63"],["dc.contributor.author","Yin, Z."],["dc.contributor.author","Raj, D."],["dc.contributor.author","Saiepour, Nasrin"],["dc.contributor.author","van Dam, D."],["dc.contributor.author","Brouwer, Nieske"],["dc.contributor.author","Eggen, Bart J. L."],["dc.contributor.author","Hanisch, U.-K."],["dc.contributor.author","Hol, E."],["dc.contributor.author","Kamphuis, W."],["dc.contributor.author","Bayer, T."],["dc.contributor.author","De Deyn, P. P."],["dc.contributor.author","Boddeke, Erik"],["dc.date.accessioned","2018-11-07T09:54:20Z"],["dc.date.available","2018-11-07T09:54:20Z"],["dc.date.issued","2015"],["dc.identifier.isi","000356386700671"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36516"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.conference","12th European Meeting on Glial Cell Function in Health and Disease"],["dc.relation.eventlocation","Bilbao, SPAIN"],["dc.relation.issn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.title","beta-amyloid plaque-associated microglia priming in transgenic mouse models of Alzheimer's disease"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.volume","63"],["dc.contributor.author","Saiepour, Nasrin"],["dc.contributor.author","Bayer, Thomas A."],["dc.contributor.author","Boddeke, Hendrikus W. G. M."],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.date.accessioned","2018-11-07T09:54:19Z"],["dc.date.available","2018-11-07T09:54:19Z"],["dc.date.issued","2015"],["dc.format.extent","E350"],["dc.identifier.isi","000356386700594"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36512"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.conference","12th European Meeting on Glial Cell Function in Health and Disease"],["dc.relation.eventlocation","Bilbao, SPAIN"],["dc.relation.issn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.title","Functional properties of microglia in mouse models of Alzheimer's disease"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","56"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Acta Neuropathologica Communications"],["dc.bibliographiccitation.volume","1"],["dc.contributor.author","Antonios, Gregory"],["dc.contributor.author","Saiepour, Nasrin"],["dc.contributor.author","Bouter, Yvonne"],["dc.contributor.author","Richard, Bernhard C."],["dc.contributor.author","Paetau, Anders"],["dc.contributor.author","Verkkoniemi-Ahola, Auli"],["dc.contributor.author","Lannfelt, Lars"],["dc.contributor.author","Ingelsson, Martin"],["dc.contributor.author","Kovacs, Gabor G."],["dc.contributor.author","Pillot, Thierry"],["dc.contributor.author","Wirths, Oliver"],["dc.contributor.author","Bayer, Thomas A."],["dc.date.accessioned","2019-07-09T11:41:53Z"],["dc.date.available","2019-07-09T11:41:53Z"],["dc.date.issued","2013"],["dc.description.abstract","Abstract Background The amyloid hypothesis in Alzheimer disease (AD) considers amyloid β peptide (Aβ) deposition causative in triggering down-stream events like neurofibrillary tangles, cell loss, vascular damage and memory decline. In the past years N-truncated Aβ peptides especially N-truncated pyroglutamate AβpE3-42 have been extensively studied. Together with full-length Aβ1–42 and Aβ1–40, N-truncated AβpE3-42 and Aβ4–42 are major variants in AD brain. Although Aβ4–42 has been known for a much longer time, there is a lack of studies addressing the question whether AβpE3-42 or Aβ4–42 may precede the other in Alzheimer’s disease pathology. Results Using different Aβ antibodies specific for the different N-termini of N-truncated Aβ, we discovered that Aβ4-x preceded AβpE3-x intraneuronal accumulation in a transgenic mouse model for AD prior to plaque formation. The novel Aβ4-x immunoreactive antibody NT4X-167 detected high molecular weight aggregates derived from N-truncated Aβ species. While NT4X-167 significantly rescued Aβ4–42 toxicity in vitro no beneficial effect was observed against Aβ1–42 or AβpE3-42 toxicity. Phenylalanine at position four of Aβ was imperative for antibody binding, because its replacement with alanine or proline completely prevented binding. Although amyloid plaques were observed using NT4X-167 in 5XFAD transgenic mice, it barely reacted with plaques in the brain of sporadic AD patients and familial cases with the Arctic, Swedish and the presenilin-1 PS1Δ9 mutation. A consistent staining was observed in blood vessels in all AD cases with cerebral amyloid angiopathy. There was no cross-reactivity with other aggregates typical for other common neurodegenerative diseases showing that NT4X-167 staining is specific for AD. Conclusions Aβ4-x precedes AβpE3-x in the well accepted 5XFAD AD mouse model underlining the significance of N-truncated species in AD pathology. NT4X-167 therefore is the first antibody reacting with Aβ4-x and represents a novel tool in Alzheimer research."],["dc.identifier.doi","10.1186/2051-5960-1-56"],["dc.identifier.pmid","24252153"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12500"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58537"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","N-truncated Abeta starting with position four: early intraneuronal accumulation and rescue of toxicity using NT4X-167, a novel monoclonal antibody"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","205"],["dc.bibliographiccitation.journal","Brain Behavior and Immunity"],["dc.bibliographiccitation.lastpage","221"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Schaafsma, W."],["dc.contributor.author","Zhang, X."],["dc.contributor.author","van Zomeren, K. C."],["dc.contributor.author","Jacobs, S."],["dc.contributor.author","Georgieva, Petya B."],["dc.contributor.author","Wolf, S. A."],["dc.contributor.author","Kettenmann, Helmut"],["dc.contributor.author","Janova, Hana"],["dc.contributor.author","Saiepour, Nasrin"],["dc.contributor.author","Hanisch, U.-K."],["dc.contributor.author","Meerlo, Peter"],["dc.contributor.author","van den Elsen, Peter J."],["dc.contributor.author","Brouwer, Nieske"],["dc.contributor.author","Boddeke, Hendrikus W. G. M."],["dc.contributor.author","Eggen, Bart J. L."],["dc.date.accessioned","2018-11-07T09:53:59Z"],["dc.date.available","2018-11-07T09:53:59Z"],["dc.date.issued","2015"],["dc.description.abstract","Microglia, the innate immune cells of the central nervous system (CNS), react to endotoxins like bacterial lipopolysaccharides (LPS) with a pronounced inflammatory response. To avoid excess damage to the CNS, the microglia inflammatory response needs to be tightly regulated. Here we report that a single LPS challenge results in a prolonged blunted pro-inflammatory response to a subsequent LPS stimulation, both in primary microglia cultures (100 ng/ml) and in vivo after intraperitoneal (0.25 and 1 mg/kg) or intracere-broventricular (5 mu g) LPS administration. Chromatin immunoprecipitation (ChIP) experiments with primary microglia and microglia acutely isolated from mice showed that LPS preconditioning was accompanied by a reduction in active histone modifications AcH3 and H3K4me3 in the promoters of the IL-10 and TNF-alpha genes. Furthermore, LPS preconditioning resulted in an increase in the amount of repressive histone modification H3K9me2 in the IL-1 beta promoter. ChIP and knock-down experiments showed that NF-kappa B subunit RelB was bound to the IL-1 beta promoter in preconditioned microglia and that RelB is required for the attenuated LPS response. In addition to a suppressed pro-inflammatory response, preconditioned primary microglia displayed enhanced phagocytic activity, increased outward potassium currents and nitric oxide production in response to a second LPS challenge. In vivo, a single i.p. LPS injection resulted in reduced performance in a spatial learning task 4 weeks later, indicating that a single inflammatory episode affected memory formation in these mice. Summarizing, we show that LPS-preconditioned microglia acquire an epigenetically regulated, immune-suppressed phenotype, possibly to prevent excessive damage to the central nervous system in case of recurrent (peripheral) inflammation. (C) 2015 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.bbi.2015.03.013"],["dc.identifier.isi","000358460700023"],["dc.identifier.pmid","25843371"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36442"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.relation.issn","1090-2139"],["dc.relation.issn","0889-1591"],["dc.title","Long-lasting pro-inflammatory suppression of microglia by LPS-preconditioning is mediated by RelB-dependent epigenetic silencing"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","115"],["dc.bibliographiccitation.journal","Neurobiology of Aging"],["dc.bibliographiccitation.lastpage","122"],["dc.bibliographiccitation.volume","55"],["dc.contributor.author","Yin, Zhuoran"],["dc.contributor.author","Raj, Divya"],["dc.contributor.author","Saiepour, Nasrin"],["dc.contributor.author","Van Dam, Debby"],["dc.contributor.author","Brouwer, Nieske"],["dc.contributor.author","Holtman, Inge R."],["dc.contributor.author","Eggen, Bart J.L."],["dc.contributor.author","Möller, Thomas"],["dc.contributor.author","Tamm, Joseph A."],["dc.contributor.author","Abdourahman, Aicha"],["dc.contributor.author","Hol, Elly M."],["dc.contributor.author","Kamphuis, Willem"],["dc.contributor.author","Bayer, Thomas A."],["dc.contributor.author","De Deyn, Peter P."],["dc.contributor.author","Boddeke, Erik"],["dc.date.accessioned","2020-12-10T15:20:27Z"],["dc.date.available","2020-12-10T15:20:27Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1016/j.neurobiolaging.2017.03.021"],["dc.identifier.issn","0197-4580"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72674"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Immune hyperreactivity of Aβ plaque-associated microglia in Alzheimer's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","911"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","922"],["dc.bibliographiccitation.volume","64"],["dc.contributor.author","Albrecht, Anne"],["dc.contributor.author","Ivens, Sebastian"],["dc.contributor.author","Papageorgiou, Ismini E."],["dc.contributor.author","Caliskan, Gursel"],["dc.contributor.author","Saiepour, Nasrin"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Richter-Levin, Gal"],["dc.contributor.author","Heinemann, Uwe"],["dc.contributor.author","Stork, Oliver"],["dc.date.accessioned","2018-11-07T10:14:00Z"],["dc.date.available","2018-11-07T10:14:00Z"],["dc.date.issued","2016"],["dc.description.abstract","Childhood trauma is a well-described risk factor for the development of stress-related psychopathology such as posttraumatic stress disorder or depression later in life. Childhood adversity can be modeled in rodents by juvenile stress (JS) protocols, resulting in impaired coping with stressful challenges in adulthood. In the current study, we investigated the long-lasting impact of JS on the expression of molecular factors for glutamate and gamma-aminobutyric acid (GABA) uptake and turnover in sublayers of the dentate gyrus (DG) using laser microdissection and quantitative real-time polymerase chain reaction. We observed reduced mRNA expression levels after JS for factors mediating astrocytic glutamate and GABA uptake and degradation. These alterations were prominently observed in the dorsal but not ventral DG granule cell layer, indicating a lasting change in astrocytic GABA and glutamate metabolism that may affect dorsal DG network activity. Indeed, we observed increased inhibition and a lack of facilitation in response to paired-pulse stimulation at short interstimulus intervals in the dorsal DG after JS, while no alterations were evident in basal synaptic transmission or forms of long-term plasticity. The shift in paired-pulse response was mimicked by pharmacologically blocking the astrocytic GABA transporter GAT-3 in naive animals. Accordingly, reduced expression levels of GAT-3 were confirmed at the protein level in the dorsal granule cell layer of rats stressed in juvenility. Together, these data demonstrate a lasting shift in the excitatory/inhibitory balance of dorsal DG network activity by JS that appears to be mediated by decreased GABA uptake into astrocytes."],["dc.identifier.doi","10.1002/glia.22970"],["dc.identifier.isi","000374326600003"],["dc.identifier.pmid","26875694"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40544"],["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","Shifts in Excitatory/Inhibitory Balance by Juvenile Stress: A Role for Neuron-Astrocyte Interaction in the Dentate Gyrus"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","635"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","649"],["dc.bibliographiccitation.volume","64"],["dc.contributor.author","Janova, Hana"],["dc.contributor.author","Böttcher, Chotima"],["dc.contributor.author","Holtman, Inge R."],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Rossum, Denise van"],["dc.contributor.author","Götz, Alexander"],["dc.contributor.author","Ernst, Anne-Sophie"],["dc.contributor.author","Fritsche, Christin"],["dc.contributor.author","Gertig, Ulla"],["dc.contributor.author","Saiepour, Nasrin"],["dc.contributor.author","Gronke, Konrad"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Rolfes, Simone"],["dc.contributor.author","Weinstein, Jonathan"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Kopatz, Jens"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Salinas-Riester, Gabriela"],["dc.contributor.author","Weber, Martin S."],["dc.contributor.author","Prinz, Marco"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Eggen, Bart J. L."],["dc.contributor.author","Boddeke, Hendrikus W. G. M."],["dc.contributor.author","Priller, Josef"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.date.accessioned","2017-09-07T11:45:34Z"],["dc.date.available","2017-09-07T11:45:34Z"],["dc.date.issued","2016"],["dc.description.abstract","Microglia, innate immune cells of the CNS, sense infection and damage through overlapping receptor sets. Toll-like receptor (TLR) 4 recognizes bacterial lipopolysaccharide (LPS) and multiple injury-associated factors. We show that its co-receptor CD14 serves three non-redundant functions in microglia. First, it confers an up to 100-fold higher LPS sensitivity compared to peripheral macrophages to enable efficient proinflammatory cytokine induction. Second, CD14 prevents excessive responses to massive LPS challenges via an interferon β-mediated feedback. Third, CD14 is mandatory for microglial reactions to tissue damage-associated signals. In mice, these functions are essential for balanced CNS responses to bacterial infection, traumatic and ischemic injuries, since CD14 deficiency causes either hypo- or hyperinflammation, insufficient or exaggerated immune cell recruitment or worsened stroke outcomes. While CD14 orchestrates functions of TLR4 and related immune receptors, it is itself regulated by TLR and non-TLR systems to thereby fine-tune microglial damage-sensing capacity upon infectious and non-infectious CNS challenges."],["dc.identifier.doi","10.1002/glia.22955"],["dc.identifier.gro","3150405"],["dc.identifier.pmid","26683584"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7166"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","0894-1491"],["dc.title","CD14 is a key organizer of microglial responses to CNS infection and injury"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1176"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","1185"],["dc.bibliographiccitation.volume","65"],["dc.contributor.author","Doering, Christin"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Gertig, Ulla"],["dc.contributor.author","van Rossum, Denise"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Saiepour, Nasrin"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Janova, Hana"],["dc.date.accessioned","2018-11-07T10:22:27Z"],["dc.date.available","2018-11-07T10:22:27Z"],["dc.date.issued","2017"],["dc.description.abstract","Microglia as principle innate immune cells of the central nervous system (CNS) are the first line of defense against invading pathogens. They are capable of sensing infections through diverse receptors, such as Toll-like receptor 4 (TLR4). This receptor is best known for its ability to recognize bacterial lipopolysaccharide (LPS), a causative agent of gram-negative sepsis and septic shock. A putative, naturally occurring antagonist of TLR4 derives from the photosynthetic bacterium Rhodobacter sphaeroides. However, the antagonistic potential of R. sphaeroides LPS (Rs-LPS) is no universal feature, since several studies suggested agonistic rather than antagonistic actions of this molecule depending on the investigated mammalian species. Here we show the agonistic versus antagonistic potential of Rs-LPS in primary mouse microglia. We demonstrate that Rs-LPS efficiently induces the release of cytokines and chemokines, which depends on TLR4, MyD88, and TRIF, but not CD14. Furthermore, Rs-LPS is able to regulate the phagocytic capacity of microglia as agonist, while it antagonizes Re-LPS-induced MHC I expression. Finally, to our knowledge, we are the first to provide in vivo evidence for an agonistic potential of Rs-LPS, as it efficiently triggers the recruitment of peripheral immune cells to the endotoxin-challenged CNS. Together, our results argue for a versatile and complex organization of the microglial TLR4 system, which specifically translates exogenous signals into cellular functions. Importantly, as demonstrated here for microglia, the antagonistic potential of Rs-LPS needs to be considered with caution, as reactions to Rs-LPS not only differ by cell type, but even by function within one cell type."],["dc.description.sponsorship","German Research Council (DFG) [SFB/TRR43, FOR1336]"],["dc.identifier.doi","10.1002/glia.23151"],["dc.identifier.isi","000401345400011"],["dc.identifier.pmid","28471051"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42277"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Wiley"],["dc.relation.issn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.title","A presumed antagonistic LPS identifies distinct functional organization of TLR4 in mouse microglia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","204"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Molecular Ecology Resources"],["dc.bibliographiccitation.lastpage","215"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Gogarten, Jan F."],["dc.contributor.author","Calvignac‐Spencer, Sébastien"],["dc.contributor.author","Nunn, Charles L."],["dc.contributor.author","Ulrich, Markus"],["dc.contributor.author","Saiepour, Nasrin"],["dc.contributor.author","Nielsen, Henrik Vedel"],["dc.contributor.author","Deschner, Tobias"],["dc.contributor.author","Fichtel, Claudia"],["dc.contributor.author","Kappeler, Peter M."],["dc.contributor.author","Knauf, Sascha"],["dc.contributor.author","Müller‐Klein, Nadine"],["dc.contributor.author","Ostner, Julia"],["dc.contributor.author","Robbins, Martha M."],["dc.contributor.author","Sangmaneedet, Somboon"],["dc.contributor.author","Schülke, Oliver"],["dc.contributor.author","Surbeck, Martin"],["dc.contributor.author","Wittig, Roman M."],["dc.contributor.author","Sliwa, Alexander"],["dc.contributor.author","Strube, Christina"],["dc.contributor.author","Leendertz, Fabian H."],["dc.contributor.author","Roos, Christian"],["dc.contributor.author","Noll, Angela"],["dc.date.accessioned","2021-04-14T08:27:47Z"],["dc.date.available","2021-04-14T08:27:47Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1111/1755-0998.13101"],["dc.identifier.eissn","1755-0998"],["dc.identifier.issn","1755-098X"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82401"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1755-0998"],["dc.relation.issn","1755-098X"],["dc.title","Metabarcoding of eukaryotic parasite communities describes diverse parasite assemblages spanning the primate phylogeny"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]