Hanisch, Uwe-Karsten

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Clinical & Experimental Metastasis"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.date.accessioned","2018-11-07T10:00:14Z"],["dc.date.available","2018-11-07T10:00:14Z"],["dc.date.issued","2015"],["dc.format.extent","231"],["dc.identifier.isi","000351601900150"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37755"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Dordrecht"],["dc.relation.issn","1573-7276"],["dc.relation.issn","0262-0898"],["dc.title","The crucial impact of the unique organ-specific defense system during colonization and outgrowth of brain metastasis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Kramann, N."],["dc.contributor.author","Menken, Lena"],["dc.contributor.author","Hayardeny, Liat"],["dc.contributor.author","Hanisch, U-K"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Wegner, C."],["dc.date.accessioned","2018-11-07T09:35:28Z"],["dc.date.available","2018-11-07T09:35:28Z"],["dc.date.issued","2014"],["dc.format.extent","382"],["dc.identifier.isi","000354441300878"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32389"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.conference","Joint ACTRIMS-ECTRIMS Meeting"],["dc.relation.eventlocation","Boston, MA"],["dc.relation.issn","1477-0970"],["dc.relation.issn","1352-4585"],["dc.title","Laquinimod treatment prevents cuprizone-induced demyelination independent of Toll-like receptor signaling via MyD88 and TRIF"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","461"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Physiological Reviews"],["dc.bibliographiccitation.lastpage","553"],["dc.bibliographiccitation.volume","91"],["dc.contributor.author","Kettenmann, Helmut"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Noda, Mami"],["dc.contributor.author","Verkhratsky, Alexei"],["dc.date.accessioned","2018-11-07T08:57:18Z"],["dc.date.available","2018-11-07T08:57:18Z"],["dc.date.issued","2011"],["dc.description.abstract","Kettenmann H, Hanisch U-K, Noda M, Verkhratsky A. Physiology of Microglia. Physiol Rev 91: 461-553, 2011; doi:10.1152/physrev.00011.2010.-Microglial cells are the resident macrophages in the central nervous system. These cells of mesodermal/mesenchymal origin migrate into all regions of the central nervous system, disseminate through the brain parenchyma, and acquire a specific ramified morphological phenotype termed \"resting microglia.\" Recent studies indicate that even in the normal brain, microglia have highly motile processes by which they scan their territorial domains. By a large number of signaling pathways they can communicate with macroglial cells and neurons and with cells of the immune system. Likewise, microglial cells express receptors classically described for brain-specific communication such as neurotransmitter receptors and those first discovered as immune cell-specific such as for cytokines. Microglial cells are considered the most susceptible sensors of brain pathology. Upon any detection of signs for brain lesions or nervous system dysfunction, microglial cells undergo a complex, multistage activation process that converts them into the \"activated microglial cell.\" This cell form has the capacity to release a large number of substances that can act detrimental or beneficial for the surrounding cells. Activated microglial cells can migrate to the site of injury, proliferate, and phagocytose cells and cellular compartments."],["dc.identifier.doi","10.1152/physrev.00011.2010"],["dc.identifier.isi","000290017800003"],["dc.identifier.pmid","21527731"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23361"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Physiological Soc"],["dc.relation.issn","1522-1210"],["dc.relation.issn","0031-9333"],["dc.title","Physiology of Microglia"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","143"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Neurosurgical Review"],["dc.bibliographiccitation.lastpage","149"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Kuhn, Susanne Antje"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Ebmeier, Kristian"],["dc.contributor.author","Beetz, Christian"],["dc.contributor.author","Brodhun, Michael"],["dc.contributor.author","Reichart, Rupert"],["dc.contributor.author","Ewald, Christian"],["dc.contributor.author","Deufel, Thomas"],["dc.contributor.author","Kalff, Rolf"],["dc.date.accessioned","2018-11-07T11:03:49Z"],["dc.date.available","2018-11-07T11:03:49Z"],["dc.date.issued","2007"],["dc.description.abstract","The case of a 7-year-old boy suffering from a supratentorial primitive neuroectodermal tumour (sPNET) at the age of 5 is presented. The tumour has been characterized by astrocytic areas within the sPNET revealing malignant transformation up to a multiform glioblastoma during the course of the disease. The clonal origin of both tumour components was established by loss of heterozygosity (LOH) analysis. Clinically, the tumour showed an aggressive biological behaviour with two recurrences. We discuss this very rare case and the first description of the clonal origin of distinct and distinguishable tumour components taking into consideration published literature."],["dc.identifier.doi","10.1007/s10143-007-0069-5"],["dc.identifier.isi","000244790200013"],["dc.identifier.pmid","17333087"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51697"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","56th Annual Meeting of the German-Society-of-Neurosurgery"],["dc.relation.eventlocation","Strasbourg, GERMANY"],["dc.relation.issn","0344-5607"],["dc.title","A paediatric supratentorial primitive neuroectodermal tumour associated with malignant astrocytic transformation and a clonal origin of both components"],["dc.type","conference_paper"],["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.journal","European Journal of Neurology"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Kuhn, S."],["dc.contributor.author","Kratzsch, Tobias"],["dc.contributor.author","Handel, Linn L."],["dc.contributor.author","Kalff, Rolf"],["dc.contributor.author","Hanisch, U.-K."],["dc.contributor.author","Vajkoczy, Peter"],["dc.date.accessioned","2018-11-07T09:56:04Z"],["dc.date.available","2018-11-07T09:56:04Z"],["dc.date.issued","2015"],["dc.format.extent","314"],["dc.identifier.isi","000357033500518"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36887"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.conference","1st Congress of the European-Academy-of-Neurology"],["dc.relation.eventlocation","Berlin, GERMANY"],["dc.relation.issn","1468-1331"],["dc.relation.issn","1351-5101"],["dc.title","From Trousseau syndrome to CoaGlio IV: the translational journey from our patients via glioblastoma biology back to a randomized, controlled multicenter trial"],["dc.type","conference_abstract"],["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.firstpage","16"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","26"],["dc.bibliographiccitation.volume","56"],["dc.contributor.author","Weinstein, Jonathan R."],["dc.contributor.author","Swarts, Sarah"],["dc.contributor.author","Bishop, Caroline"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Moeller, Thomas"],["dc.date.accessioned","2018-11-07T11:19:59Z"],["dc.date.available","2018-11-07T11:19:59Z"],["dc.date.issued","2008"],["dc.description.abstract","Lipopolysaccharide (LPS/endotoxin) is a potent immunologic stimulant. Many commercial-grade reagents used in research are not screened for LPS contamination. LPS induces a wide spectrum of proinflammatory responses in microglia, the immune cells of the brain. Recent studies have demonstrated that a broad range of endogenous factors including plasma-derived proteins and bioactive phospholipids can also activate microglia. However, few of these studies have reported either the LPS levels found in the preparations used or the effect of LPS inhibitors such as polymyxin B (PMX) on factor-induced responses. Here, we used the Limulus amoebocyte lysate assay to screen a broad range of commercial- and pharmaceutical-grade proteins, peptides, lipids, and inhibitors commonly used in microglia research for contamination with LPS. We then characterized the ability of PMX to alter a representative set of factor-induced microglial activation parameters including surface antigen expression, metabolic activity/proliferation, and NO/cytokine/chemokine release in both the N9 microglial cell line and primary microglia. Significant levels of LPS contamination were detected in a number of commercial-grade plasma/serum- and nonplasma/serum-derived proteins, phospholipids, and synthetic peptide preparations, but not in pharmaceutical-grade recombinant proteins or pharmacological inhibitors. PMX had a significant inhibitory effect on the microglia-activating potential of a number of commercial-, but not pharmaceutical-grade, protein preparations. Novel PMX-resistant responses to alpha(2)-macroglobulin and albumin were incidentally observed. Our results indicate that LPS is a frequent and significant contaminant in commercial-grade preparations of previously reported microglia-activating factors. Careful attention to LPS levels and appropriate controls are necessary or future studies in the neuroinflammation field. (c) 2007 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/glia.20585"],["dc.identifier.isi","000251469100002"],["dc.identifier.pmid","17910052"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55423"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0894-1491"],["dc.title","Lipopolysaccharide is a frequent and significant contaminant in microglia-activating factors"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]