Algner, Michaela

[["dc.bibliographiccitation.journal","International Journal of Medical Microbiology"],["dc.bibliographiccitation.volume","294"],["dc.contributor.author","Lang, C."],["dc.contributor.author","Algner, M."],["dc.contributor.author","Gross, U."],["dc.contributor.author","Luder, C. G. K."],["dc.date.accessioned","2018-11-07T10:45:58Z"],["dc.date.available","2018-11-07T10:45:58Z"],["dc.date.issued","2004"],["dc.format.extent","120"],["dc.identifier.isi","000224456000084"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47632"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Urban & Fischer Verlag"],["dc.publisher.place","Jena"],["dc.relation.conference","Annual Meeting of the DGHM"],["dc.relation.eventlocation","Munster, GERMANY"],["dc.relation.issn","1438-4221"],["dc.title","Differential effects of Toxoplasma gondii and parasite lysate on GAS-containing promoters driving IFN-gamma-responsive genes"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","833"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","International Journal for Parasitology"],["dc.bibliographiccitation.lastpage","844"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Luder, Carsten G. K."],["dc.contributor.author","Algner, Michaela"],["dc.contributor.author","Lang, Christine"],["dc.contributor.author","Bleicher, Nadja"],["dc.contributor.author","Groß, Uwe"],["dc.date.accessioned","2018-11-07T10:37:35Z"],["dc.date.available","2018-11-07T10:37:35Z"],["dc.date.issued","2003"],["dc.description.abstract","Production of nitric oxide by activated murine macrophages is thought to represent an important mechanism to restrict replication of the obligate intracellular parasite Toxoplasma gondii. In this study, we characterised the effect of T. gondii on nitric oxide production and expression of the inducible nitric oxide synthase and determined the functional significance of a parasite-induced evasion of this potential effector mechanism. Infection of primary bone marrow-derived macrophages or monocytic/macrophage RAW264.7 cells with a mouse-avirulent T. gondii strain significantly decreased nitric oxide production that had been induced by activation with either interferon-gamma or lipopolysaccharide or interferon-gamma plus lipopolysaccharide. Importantly, down-regulation of nitric oxide production by T. gondii enabled considerable parasite replication in macrophages activated with interferon-gamma alone or lipopolysaccharide, alone. Furthermore, supplementation of endogenous nitric oxide by addition of sodium nitroprusside to levels as observed in uninfected interferon-gamma- or lipopolysaccharide-activated macrophages almost completely abrogated replication of T. gondii. Although T. gondii also partially inhibited the vigorous nitric oxide production induced by interferon-gamma along with lipopolysaccharide, the magnitude of inhibition did not suffice to allow intracellular propagation of the parasite in these synergistically activated macrophages. Inhibition of interferon-gamma-, lipopolysaccharide- and interferon--y plus lipopolysaccharide-induced nitric oxide production coincided with reduced inducible nitric oxide synthase protein levels. Such down-regulation required the presence of intracellular parasites as determined by immunofluorescence microscopy. Inducible nitric oxide synthase transcripts induced by interferon--y alone or in combination with lipopolysaccharide were also dose-dependently down-regulated after infection of RAW264.7 cells with T gondii. In conclusion, this evasion strategy enables parasite replication in macrophages moderately activated by interferon-gamma or lipopolysaccharide, but does not suffice to evade the anti-parasitic activity of macrophages fully activated by interferon-gamma plus lipopolysaccharide. Nitric oxide production and its partial inhibition by the parasite may modulate the parasite-host equilibrium during toxoplasmosis. (C) 2003 Australian Society for Parasitology Inc. Published by Elsevier Science Ltd. All rights reserved."],["dc.identifier.doi","10.1016/S0020-7519(03)00092-4"],["dc.identifier.isi","000184375800007"],["dc.identifier.pmid","12865083"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45603"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","Najko"],["dc.relation.issn","0020-7519"],["dc.title","Reduced expression of the inducible nitric oxide synthase after infection with Toxoplasma gondii facilitates parasite replication in activated murine macrophages"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1994"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Microbes and Infection"],["dc.bibliographiccitation.lastpage","2005"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Lang, Christine"],["dc.contributor.author","Algner, Michaela"],["dc.contributor.author","Beinert, Nicole"],["dc.contributor.author","Gross, Uwe"],["dc.contributor.author","Lueder, Carsten Guenter Kurt"],["dc.date.accessioned","2018-11-07T09:38:13Z"],["dc.date.available","2018-11-07T09:38:13Z"],["dc.date.issued","2006"],["dc.description.abstract","The intracellular parasite Toxoplasma gondii is able to establish persistent infections in immunocompetent hosts and this may be facilitated by different immune evasion mechanisms. In the present study, we describe that infection of marine monocyte/macrophage RAW 264.7 cells with T. gondii blocks the IFN-gamma-induced upregulation of major histocompatibility complex (MHC) class II mRNAs and proteins. Heat inactivation of the parasites prior to host cell invasion, but not inhibition of the intracellular replication of T. gondii abolished the inhibition of MHC class II upregulation. Interestingly, a T. gondii lysate (TL) mimicked the inhibitory effect of viable parasites on MHC class II expression. Nuclear translocation of the signal transducer and activator of transcription in response to IFN-gamma were normal both in cells incubated with TL or infected with viable parasites. Transcript levels of the class II transactivator and consequently H2-Ab were nevertheless diminished by both viable parasites and TL. In contrast, interferon regulatory factor-1 mRNA was only decreased in response to viable T. gondii. Luciferase reporter assays confirmed differential effects of viable parasites and TL on minimal or complex IFN-gamma-responsive promoters. Furthermore, only TL, and not viable parasites, strongly induced the secretion of IL-10 by marine macrophages. Whereas TL also inhibited MHC class II expression in macrophages from IL-10-deficient mice, increased IL-10 secretion by wild type macrophages did not mediate the block in MHC class II upregulation. In conclusion, T. gondii employs different mechanisms to inhibit MHC class II expression, suggesting a complex regulation of this immune evasion strategy. (c) 2006 Elsevier SAS. All rights reserved."],["dc.identifier.doi","10.1016/j.micinf.2006.02.031"],["dc.identifier.isi","000241115100002"],["dc.identifier.pmid","16824778"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33024"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1286-4579"],["dc.title","Diverse mechanisms employed by Toxoplasma gondii to inhibit IFN-gamma-induced major histocompatibility complex class II gene expression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","International Journal of Medical Microbiology"],["dc.bibliographiccitation.volume","293"],["dc.contributor.author","Lang, C."],["dc.contributor.author","Algner, M."],["dc.contributor.author","Gross, U."],["dc.contributor.author","Luder, C. G. K."],["dc.date.accessioned","2018-11-07T10:50:39Z"],["dc.date.available","2018-11-07T10:50:39Z"],["dc.date.issued","2004"],["dc.format.extent","74"],["dc.identifier.isi","000222589900078"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48706"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Urban & Fischer Verlag"],["dc.publisher.place","Jena"],["dc.relation.conference","21st Congress of the German-Society-of-Parasitology"],["dc.relation.eventlocation","Univ Wurzburg, Wurzburg, GERMANY"],["dc.relation.issn","1438-4221"],["dc.title","Diverse mechanisms of Toxoplasma gondii to interfere with the IFN-gamma-induced MHC class II expression in murine macrophages"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","PII S0165-5728(02)00320-X"],["dc.bibliographiccitation.firstpage","12"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","24"],["dc.bibliographiccitation.volume","134"],["dc.contributor.author","Luder, C. G. K."],["dc.contributor.author","Lang, C."],["dc.contributor.author","Giraldo-Velasquez, M."],["dc.contributor.author","Algner, M."],["dc.contributor.author","Gerdes, Jan S."],["dc.contributor.author","Gross, U."],["dc.date.accessioned","2018-11-07T10:42:35Z"],["dc.date.available","2018-11-07T10:42:35Z"],["dc.date.issued","2003"],["dc.description.abstract","Major histocompatibility complex (MHC) class II expression by microglia and astrocytes is critical for CD4+-mediated immune responses within the central nervous system. Here, we demonstrate that the obligate intracellular parasite, Toxoplasma gondii, down-regulates activation-induced MHC class II expression in human-derived glioblastoma cells as well as in primary astrocytes and microglia from cortices of rat fetuses. Down-regulation of MHC class II proteins was predominantly observed in parasite-positive, but not parasite-negative, host cells of T gondii-infected cell cultures. MHC class II transcript levels induced by IFN-gamma alone or in combination with TNF-alpha were also clearly diminished after parasitic infection. Furthermore, T gondii dose-dependently down-regulated the transcript levels of the class II transactivator CIITA. These results suggest that T. gondii partially evade CD4+-mediated intracerebral immune responses, a mechanism which may contribute to long-term persistence of the parasite within the CNS. (C) 2002 Elsevier Science B.V. All rights reserved."],["dc.identifier.doi","10.1016/S0165-5728(02)00320-X"],["dc.identifier.isi","000180508700002"],["dc.identifier.pmid","12507768"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/46831"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0165-5728"],["dc.title","Toxoplasma gondii inhibits MHC class II expression in neural antigen-presenting cells by down-regulating the class II transactivator CIITA"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]