Regen, Tommy

[["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.firstpage","1587"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Cancer Immunology Immunotherapy"],["dc.bibliographiccitation.lastpage","1597"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Koenig, Simone"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Dittmann, Kai"],["dc.contributor.author","Engelke, Michael"],["dc.contributor.author","Wienands, Juergen"],["dc.contributor.author","Schwendener, Reto"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Hahn, Heidi"],["dc.date.accessioned","2018-11-07T09:19:32Z"],["dc.date.available","2018-11-07T09:19:32Z"],["dc.date.issued","2013"],["dc.description.abstract","Liposomes are frequently used in cancer therapy to encapsulate and apply anticancer drugs. Here, we show that a systemic treatment of mice bearing skin tumors with empty phosphatidylcholine liposomes (PCL) resulted in inhibition of tumor growth, which was similar to that observed with the synthetic bacterial lipoprotein and TLR1/2 agonist Pam(3)CSK(4) (BLP). Both compounds led to a substantial decrease of macrophages in spleen and in the tumor-bearing skin. Furthermore, both treatments induced the expression of typical macrophage markers in the tumor-bearing tissue. As expected, BLP induced the expression of the M1 marker genes Cxcl10 and iNOS, whereas PCL, besides inducing iNOS, also increased the M2 marker genes Arg1 and Trem2. In vitro experiments demonstrated that neither PCL nor BLP influenced proliferation or survival of tumor cells, whereas both compounds inhibited proliferation and survival and increased the migratory capacity of bone marrow-derived macrophages (BMDM). However, in contrast to BLP, PCL did not activate cytokine secretion and induced a different BMDM phenotype. Together, the data suggest that similar to BLP, PCL induce an antitumor response by influencing the tumor microenvironment, in particular by functional alterations of macrophages, however, in a distinct manner from those induced by BLP."],["dc.description.sponsorship","DFG [FOR942 HA 2197/5-2]"],["dc.identifier.doi","10.1007/s00262-013-1444-4"],["dc.identifier.isi","000325008800005"],["dc.identifier.pmid","23917775"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28662"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0340-7004"],["dc.title","Empty liposomes induce antitumoral effects associated with macrophage responses distinct from those of the TLR1/2 agonist Pam(3)CSK(4) (BLP)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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.firstpage","447"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Cell Science"],["dc.bibliographiccitation.lastpage","458"],["dc.bibliographiccitation.volume","124"],["dc.contributor.author","Fitzner, Dirk"],["dc.contributor.author","Schnaars, Mareike"],["dc.contributor.author","van Rossum, Denise"],["dc.contributor.author","Krishnamoorthy, Gurumoorthy"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Bakhti, Mostafa"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Simons, Mikael"],["dc.date.accessioned","2018-11-07T08:59:39Z"],["dc.date.available","2018-11-07T08:59:39Z"],["dc.date.issued","2011"],["dc.description.abstract","The transfer of antigens from oligodendrocytes to immune cells has been implicated in the pathogenesis of autoimmune diseases. Here, we show that oligodendrocytes secrete small membrane vesicles called exosomes, which are specifically and efficiently taken up by microglia both in vitro and in vivo. Internalisation of exosomes occurs by a macropinocytotic mechanism without inducing a concomitant inflammatory response. After stimulation of microglia with interferon-gamma, we observe an upregulation of MHC class II in a subpopulation of microglia. However, exosomes are preferentially internalised in microglia that do not seem to have antigen-presenting capacity. We propose that the constitutive macropinocytotic clearance of exosomes by a subset of microglia represents an important mechanism through which microglia participate in the degradation of oligodendroglial membrane in an immunologically 'silent' manner. By designating the capacity for macropinocytosis and antigen presentation to distinct cells, degradation and immune function might be assigned to different subtypes of microglia."],["dc.description.sponsorship","ERC; EMBO YIP; German Research Council [SFB/TR43]"],["dc.identifier.doi","10.1242/jcs.074088"],["dc.identifier.isi","000286223600016"],["dc.identifier.pmid","21242314"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8034"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23953"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Company Of Biologists Ltd"],["dc.relation.issn","0021-9533"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Selective transfer of exosomes from oligodendrocytes to microglia by macropinocytosis"],["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.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","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"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cytokine"],["dc.bibliographiccitation.volume","43"],["dc.contributor.author","Scheffel, Joerg"],["dc.contributor.author","Rossum van, Denise"],["dc.contributor.author","Weinstein, Jonathan R."],["dc.contributor.author","Dihazi, Hassan"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Kettenmann, Helmut"],["dc.contributor.author","Prinz, Marco R."],["dc.contributor.author","Moeller, Thomas"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.date.accessioned","2018-11-07T11:11:15Z"],["dc.date.available","2018-11-07T11:11:15Z"],["dc.date.issued","2008"],["dc.format.extent","315"],["dc.identifier.doi","10.1016/j.cyto.2008.07.386"],["dc.identifier.isi","000260212900351"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53386"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Ltd Elsevier Science Ltd"],["dc.publisher.place","London"],["dc.relation.conference","7th Joint Conference of the International-Cytokine-Society/International-Society-for-Interferon-and- Cytoklin-Research"],["dc.relation.eventlocation","Montreal, CANADA"],["dc.relation.issn","1043-4666"],["dc.title","Toll-like receptor 4/MyD88 pathway mediates microglial proinflammatory cytokine responses to thrombin-associated coagulation protein complexes"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","411"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","424"],["dc.bibliographiccitation.volume","124"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Pfoertner, Ramona"],["dc.contributor.author","Pham, Trinh"],["dc.contributor.author","Zhang, J."],["dc.contributor.author","Hayardeny, Liat"],["dc.contributor.author","Piryatinsky, Victor"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Rossum, Denise van"],["dc.contributor.author","Brakelmann, Lars"],["dc.contributor.author","Hagemeier, Karin"],["dc.contributor.author","Kuhlmann, Tanja"],["dc.contributor.author","Stadelmann-Nessler, Christine"],["dc.contributor.author","John, Gareth R."],["dc.contributor.author","Kramann, Nadine"],["dc.contributor.author","Wegner, Christiane"],["dc.date.accessioned","2018-11-07T09:06:50Z"],["dc.date.available","2018-11-07T09:06:50Z"],["dc.date.issued","2012"],["dc.description.abstract","Laquinimod (LAQ) is a new oral immunomodulatory compound that reduces relapse rate, brain atrophy and disability progression in multiple sclerosis (MS). LAQ has well-documented effects on inflammation in the periphery, but little is known about its direct activity within the central nervous system (CNS). To elucidate the impact of LAQ on CNS-intrinsic inflammation, we investigated the effects of LAQ on cuprizone-induced demyelination in mice in vivo and on primary CNS cells in vitro. Demyelination, inflammation, axonal damage and glial pathology were evaluated in LAQ-treated wild type and Rag-1-deficient mice after cuprizone challenge. Using primary cells we tested for effects of LAQ on oligodendroglial survival as well as on cytokine secretion and NF-kappa B activation in astrocytes and microglia. LAQ prevented cuprizone-induced demyelination, microglial activation, axonal transections, reactive gliosis and oligodendroglial apoptoses in wild type and Rag-1-deficient mice. LAQ significantly decreased pro-inflammatory factors in stimulated astrocytes, but not in microglia. Oligodendroglial survival was not affected by LAQ in vitro. Astrocytic, but not microglial, NF-kappa B activation was markedly reduced by LAQ as evidenced by NF-kappa B reporter assay. LAQ also significantly decreased astrocytic NF-kappa B activation in cuprizone-treated mice. Our data indicate that LAQ prevents cuprizone-induced demyelination by attenuating astrocytic NF-kappa B activation. These effects are CNS-intrinsic and not mediated by peripheral immune cells. Therefore, LAQ downregulation of the astrocytic pro-inflammatory response may be an important mechanism underlying its protective effects on myelin, oligodendrocytes and axons. Modulation of astrocyte activation may be an attractive therapeutic target to prevent tissue damage in MS."],["dc.identifier.doi","10.1007/s00401-012-1009-1"],["dc.identifier.isi","000307757200010"],["dc.identifier.pmid","22766690"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9468"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25641"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0001-6322"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.title","Reduced astrocytic NF-kappa B activation by laquinimod protects from cuprizone-induced demyelination"],["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","354"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cell Host & Microbe"],["dc.bibliographiccitation.lastpage","365.e5"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Remy, Melissa M."],["dc.contributor.author","Sahin, Mehmet"],["dc.contributor.author","Flatz, Lukas"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Xu, Lifen"],["dc.contributor.author","Kreutzfeldt, Mario"],["dc.contributor.author","Fallet, Benedict"],["dc.contributor.author","Doras, Camille"],["dc.contributor.author","Rieger, Toni"],["dc.contributor.author","Bestmann, Lukas"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Kaufmann, Beat A."],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Pinschewer, Daniel D."],["dc.date.accessioned","2020-12-10T14:23:06Z"],["dc.date.available","2020-12-10T14:23:06Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1016/j.chom.2017.07.008"],["dc.identifier.issn","1931-3128"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71834"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Interferon-γ-Driven iNOS: A Molecular Pathway to Terminal Shock in Arenavirus Hemorrhagic Fever"],["dc.type","journal_article"],["dc.type.internalPublication","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"]]