Britta Burkhardt
University of Tübingen
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Britta Burkhardt.
Hepatology International | 2013
Georg Damm; Elisa Pfeiffer; Britta Burkhardt; Jan Vermehren; Andreas K. Nussler; Thomas Weiss
Many reports describing parenchymal liver cell isolation have been published so far. However, recent evidence has clearly demonstrated that non-parenchymal liver cells play an important role in many pathophysiologies of the liver, such as drug-induced liver diseases, inflammation, and the development of liver fibrosis and cirrhosis. In this study, we present an overview of the current methods for isolating and characterizing parenchymal and non-parenchymal liver cells.
Microarrays | 2015
Anastasia Bachmann; Matthias Moll; Eric Gottwald; Cordula Nies; Roman Zantl; Helga Wagner; Britta Burkhardt; Juan J. Martínez Sánchez; Ruth Ladurner; Wolfgang E. Thasler; Georg Damm; Andreas K. Nussler
One of the main challenges in drug development is the prediction of in vivo toxicity based on in vitro data. The standard cultivation system for primary human hepatocytes is based on monolayer cultures, even if it is known that these conditions result in a loss of hepatocyte morphology and of liver-specific functions, such as drug-metabolizing enzymes and transporters. As it has been demonstrated that hepatocytes embedded between two sheets of collagen maintain their function, various hydrogels and scaffolds for the 3D cultivation of hepatocytes have been developed. To further improve or maintain hepatic functions, 3D cultivation has been combined with perfusion. In this manuscript, we discuss the benefits and drawbacks of different 3D microfluidic devices. For most systems that are currently available, the main issues are the requirement of large cell numbers, the low throughput, and expensive equipment, which render these devices unattractive for research and the drug-developing industry. A higher acceptance of these devices could be achieved by their simplification and their compatibility with high-throughput, as both aspects are of major importance for a user-friendly device.
Mediators of Inflammation | 2015
Victoria Kegel; Elisa Pfeiffer; Britta Burkhardt; Jia L. Liu; Katrin Zeilinger; Andreas K. Nussler; Daniel Seehofer; Georg Damm
Drug induced liver injury (DILI) is an idiosyncratic adverse drug reaction leading to severe liver damage. Kupffer cells (KC) sense hepatic tissue stress/damage and therefore could be a tool for the estimation of consequent effects associated with DILI. Aim of the present study was to establish a human in vitro liver model for the investigation of immune-mediated signaling in the pathogenesis of DILI. Hepatocytes and KC were isolated from human liver specimens. The isolated KC yield was 1.2 ± 0.9 × 106 cells/g liver tissue with a purity of >80%. KC activation was investigated by the measurement of reactive oxygen intermediates (ROI, DCF assay) and cell activity (XTT assay). The initial KC activation levels showed broad donor variability. Additional activation of KC using supernatants of hepatocytes treated with hepatotoxic drugs increased KC activity and led to donor-dependent changes in the formation of ROI compared to KC incubated with supernatants from untreated hepatocytes. Additionally, a compound- and donor-dependent increase in proinflammatory cytokines or in anti-inflammatory cytokines was detected. In conclusion, KC related immune signaling in hepatotoxicity was successfully determined in a newly established in vitro liver model. KC were able to detect hepatocyte stress/damage and to transmit a donor- and compound-dependent immune response via cytokine production.
Excli Journal | 2015
Wei Yang; Britta Burkhardt; Luise Fischer; Maja Beirow; Nadja Bork; Eva C. Wönne; Cornelia Wagner; Bettina Husen; Katrin Zeilinger; Liegang Liu; Andreas K. Nussler
Aging is characterized by a progressive decrease of cellular functions, because cells gradually lose their capacity to respond to injury. Increased oxidative stress is considered to be one of the major contributors to age-related changes in all organs including the liver. Our study has focused on elucidating whether important antioxidative enzymes, the mTOR pathway, and MAPKs exhibit age-dependent changes in the liver of rats during aging. We found an age-dependent increase of GSH in the cytosol and mitochondria. The aged liver showed an increased SOD enzyme activity, while the CAT enzyme activity decreased. HO-1 and NOS-2 gene expression was lower in adult rats, but up-regulated in aged rats. Western blot analysis revealed that SOD1, SOD2, GPx, GR, γ-GCL, and GSS were age-dependent up-regulated, while CAT remained constant. We also demonstrated that the phosphorylation of Akt, JNK, p38, and TSC2Ser1254 decreased while ERK1/2 and TSC2Thr1462 increased age-dependently. Furthermore, our data show that the mTOR pathway seems to be activated in livers of aged rats, and hence stimulating cell proliferation/regeneration, as confirmed by an age-dependent increase of PCNA and p-eIF4ESer209 protein expression. Our data may help to explain the fact that liver cells only proliferate in cases of necessity, like injury and damage. In summary, we have demonstrated that, age-dependent changes of the antioxidant system and stress-related signaling pathways occur in the livers of rats, which may help to better understand organ aging.
Archives of Toxicology | 2013
Lilianna Schyschka; J. J. Martínez Sánchez; Z. Wang; Britta Burkhardt; U. Müller-Vieira; Katrin Zeilinger; Anastasia Bachmann; S. Nadalin; Georg Damm; Andreas K. Nussler
Hepatology International | 2014
Britta Burkhardt; Juan José Martinez-Sanchez; Anastasia Bachmann; Ruth Ladurner; Andreas K. Nussler
Archives of Toxicology | 2014
Sabrina Ehnert; Thomas Freude; Carmen Eicher; Britta Burkhardt; Juan J. Martínez Sánchez; Jan Neumann; Ruben Mühl-Benninghaus; Steven Dooley; Stefan Pscherer; Andreas K. Nussler
Advances in Bioscience and Biotechnology | 2012
Sabrina Ehnert; Stefan Döbele; Karl F. Braun; Britta Burkhardt; Valeska Hofmann; Mario Hausmann; José T. Egaña; Ulrich Stöckle; Thomas Freude; Andreas K. Nussler
Archive | 2015
Wei Yang; Britta Burkhardt; Luise Fischer; Maja Beirow; Nadja Bork; Eva C. Wönne; Cornelia Wagner; Bettina Husen; Katrin Zeilinger; Liegang Liu; Andreas K. Nussler; Eberhard Karls
Zeitschrift Fur Gastroenterologie | 2014
E Pfeiffer; V Kegel; Britta Burkhardt; Daniel Seehofer; Andreas K. Nussler; Georg Damm