Czesnik, Dirk

[["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","32"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","34"],["dc.bibliographiccitation.volume","244"],["dc.contributor.author","Redlich, Sandra"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Schuetze, Sandra"],["dc.contributor.author","Czesnik, Dirk"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2018-11-07T09:12:37Z"],["dc.date.available","2018-11-07T09:12:37Z"],["dc.date.issued","2012"],["dc.description.abstract","The ability of microglial cells to phagocytose bacteria after stimulation with the endocannabinoid palmitoylethanolamide (PEA) was studied in vitro. PEA increased the phagocytosis of unencapsulated Streptococcus pneumoniae R6 and encapsulated Escherichia coli K1 by murine microglial cells significantly after 30 min of microglial. stimulation. This suggested that stimulation of microglial cells by PEA can increase the resistance of the brain against CNS infections. (C) 2012 Elsevier B.V. All rights reserved."],["dc.description.sponsorship","European Community [223111]"],["dc.identifier.doi","10.1016/j.jneuroim.2011.12.013"],["dc.identifier.isi","000302436300005"],["dc.identifier.pmid","22244572"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26980"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0165-5728"],["dc.title","Palmitoylethanolamide stimulates phagocytosis of Escherichia coli K1 and Streptococcus pneumoniae R6 by microglial cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","53"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","54"],["dc.bibliographiccitation.volume","253"],["dc.contributor.author","Djukic, M."],["dc.contributor.author","Mildner, Alexander"],["dc.contributor.author","Schmidt, H."],["dc.contributor.author","Czesnik, D."],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Priller, Josef"],["dc.contributor.author","Nau, R."],["dc.contributor.author","Prinz, Marco R."],["dc.date.accessioned","2018-11-07T09:53:38Z"],["dc.date.available","2018-11-07T09:53:38Z"],["dc.date.issued","2006"],["dc.identifier.isi","000238478600194"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36368"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.publisher.place","Darmstadt"],["dc.relation.conference","16th Annual Meeting of the European-Neurological-Society"],["dc.relation.eventlocation","Lausanne, SWITZERLAND"],["dc.relation.issn","0340-5354"],["dc.title","Bone marrow-derived monocytes/macrophages migrate into the cental nervous system and differentiate to microglia after Streptococcus pneumoniae meningitis in mice"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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"]]

[["dc.bibliographiccitation.firstpage","2394"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","2403"],["dc.bibliographiccitation.volume","129"],["dc.contributor.author","Djukic, Marija"],["dc.contributor.author","Mildner, Alexander"],["dc.contributor.author","Schmidt, Hauke"],["dc.contributor.author","Czesnik, Dirk"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Priller, Josef"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Prinz, Marco R."],["dc.date.accessioned","2018-11-07T09:17:35Z"],["dc.date.available","2018-11-07T09:17:35Z"],["dc.date.issued","2006"],["dc.description.abstract","Previous studies have demonstrated a potential role of brain endogenous microglia and meningeal macrophages in inflammation and brain injury during bacterial meningitis. However, the contribution of previously engrafted monocytes and microglia to this process is still unknown. We therefore used genetically labelled bone marrow-derived cells from transgenic mice expressing the green fluorescent protein (GFP) under the chicken beta-actin promoter to deliver fluorescently labelled monocytes to the diseased brain. Approximately 24 hours after Streptococcus pneumoniae infection, GFP-expressing parenchymal microglia changed their morphology to an activated phenotype and upregulated major histocompatibility complex class II molecules. Bacterial meningitis increased the engraftment of GFP(+) monocytes and their differentiation to microglia during the post-inflammatory period, but not during acute meningitis. Importantly, these newly recruited monocytes became an integral part of the pool of parenchymal microglia and contributed to the clearance of damaged tissue by increased lysosomal activity and close location to apoptotic cells. Thus, circulating cells entering the brain such as monocytes/macrophages might provide a potential cellular target for the treatment of the tissue damage following meningitis via peripheral cell therapy."],["dc.identifier.doi","10.1093/brain/awl206"],["dc.identifier.isi","000240679700015"],["dc.identifier.pmid","16891321"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7750"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28202"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Circulating monocytes engraft in the brain, differentiate into microglia and contribute to the pathology following meningitis in mice"],["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","557"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Infection and Immunity"],["dc.bibliographiccitation.lastpage","564"],["dc.bibliographiccitation.volume","77"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Czesnik, Dirk"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Zeug, Andre"],["dc.contributor.author","Bukowski, Stephanie"],["dc.contributor.author","Mildner, Alexander"],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Hammerschmidt, Sven"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2018-11-07T08:34:37Z"],["dc.date.available","2018-11-07T08:34:37Z"],["dc.date.issued","2009"],["dc.description.abstract","Meningitis and meningoencephalitis caused by Escherichia coli are associated with high rates of mortality. When an infection occurs, Toll-like receptors (TLRs) expressed by microglial cells can recognize pathogen-associated molecular patterns and activate multiple steps in the inflammatory response that coordinate the brain's local defense, such as phagocytosis of invading pathogens. An upregulation of the phagocytic ability of reactive microglia could improve the host defense in immunocompromised patients against pathogens such as E. coli. Here, murine microglial cultures were stimulated with the TLR agonists Pam(3)CSK(4) (TLR1/TLR2), lipopolysaccharide (TLR4), and CpG oligodeoxynucleotide (TLR9) for 24 h. Upon stimulation, levels of tumor necrosis factor alpha and the neutrophil chemoattractant CXCL1 were increased, indicating microglial activation. Phagocytic activity was studied after adding either E. coli DH5 alpha or E. coli K1 strains. After 60 and 90 min of bacterial exposure, the number of ingested bacteria was significantly higher in cells prestimulated with TLR agonists than in unstimulated controls (P < 0.01). Addition of cytochalasin D, an inhibitor of actin polymerization, blocked >90% of phagocytosis. We also analyzed the ability of microglia to kill the ingested E. coli strains. Intracellularly surviving bacteria were quantified at different time points (90, 150, 240, and 360 min) after 90 min of phagocytosis. The number of bacteria killed intracellularly after 6 h was higher in cells primed with the different TLR agonists than in unstimulated microglia. Our data suggest that microglial stimulation by the TLR system can increase bacterial phagocytosis and killing. This approach could improve central nervous system resistance to infections in immunocompromised patients."],["dc.identifier.doi","10.1128/IAI.00903-08"],["dc.identifier.isi","000262776100058"],["dc.identifier.pmid","18981243"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7765"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17860"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Microbiology"],["dc.relation.issn","0019-9567"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Toll-Like Receptor Prestimulation Increases Phagocytosis of Escherichia coli DH5 alpha and Escherichia coli K1 Strains by Murine Microglial Cells"],["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"]]