@article{EdlichVolzBrodwolfetal.2018,
  author    = {Edlich, Alexander and Volz, Pierre and Brodwolf, Robert and Unbehauen, Michael and Mundhenk, Lars and Gruber, Achim D. and Hedtrich, Sarah and Haag, Rainer and Alexiev, Ulrike and Kleuser, Burkhard},
  title     = {Crosstalk between core-multishell nanocarriers for cutaneous drug delivery and antigen-presenting cells of the skin},
  series = {Biomaterials : biomaterials reviews online},
  volume    = {162},
  journal   = {Biomaterials : biomaterials reviews online},
  publisher = {Elsevier},
  address   = {Oxford},
  issn      = {0142-9612},
  doi       = {10.1016/j.biomaterials.2018.01.058},
  pages     = {60 -- 70},
  year      = {2018},
  abstract  = {Owing their unique chemical and physical properties core-multishell (CMS) nanocarriers are thought to underlie their exploitable biomedical use for a topical treatment of skin diseases. This highlights the need to consider not only the efficacy of CMS nanocarriers but also the potentially unpredictable and adverse consequences of their exposure thereto. As CMS nanocarriers are able to penetrate into viable layers of normal and stripped human skin ex vivo as well as in in vitro skin disease models the understanding of nanoparticle crosstalk with components of the immune system requires thorough investigation. Our studies highlight the biocompatible properties of CMS nanocarriers on Langerhans cells of the skin as they did neither induce cytotoxicity and genotoxicity nor cause reactive oxygen species (ROS) or an immunological response. Nevertheless, CMS nanocarriers were efficiently taken up by Langerhans cells via divergent endocytic pathways. Bioimaging of CMS nanocarriers by fluorescence lifetime imaging microscopy (FLIM) and flow cytometry indicated not only a localization within the lysosomes but also an energy-dependent exocytosis of unmodified CMS nanocarriers into the extracellular environment. (C) 2018 Elsevier Ltd. All rights reserved.},
  language  = {en}
}
@misc{PischonRadbruchOstrowskietal.2017,
  author    = {Pischon, Hannah and Radbruch, Moritz and Ostrowski, Anja and Schumacher, Fabian and Hoenzke, Stefan and Kleuser, Burkhard and Hedtrich, Sarah and Fluhr, Joachim W. and Gruber, Achim D. and Mundhenk, Lars},
  title     = {How Effective Is Tacrolimus in the Imiquimod},
  series = {The journal of investigative dermatology},
  volume    = {138},
  journal   = {The journal of investigative dermatology},
  number    = {2},
  publisher = {Elsevier},
  address   = {New York},
  issn      = {0022-202X},
  doi       = {10.1016/j.jid.2017.09.019},
  pages     = {455 -- 458},
  year      = {2017},
  language  = {en}
}
@article{SzymanskiToenniesBecheretal.2012,
  author    = {Szymanski, Kolja V. and T{\"o}nnies, Mario and Becher, Anne and Fatykhova, Diana and N'Guessan, Philippe D. and Gutbier, Birgitt and Klauschen, Frederick and Neusch{\"a}fer-Rube, Frank and Schneider, Paul and R{\"u}ckert, Jens and Neudecker, Jens and Bauer, Torsten T. and Dalhoff, Klaus and Droemann, Daniel and Gruber, Achim D. and Kershaw, Olivia and Temmesfeld-Wollbrueck, Bettina and Suttorp, Norbert and Hippenstiel, Stefan and Hocke, Andreas C.},
  title     = {Streptococcus pneumoniae-induced regulation of cyclooxygenase-2 in human lung tissue},
  series = {The European respiratory journal : official journal of the European Society for Clinical Respiratory Physiology},
  volume    = {40},
  journal   = {The European respiratory journal : official journal of the European Society for Clinical Respiratory Physiology},
  number    = {6},
  publisher = {European Respiratory Society},
  address   = {Sheffield},
  issn      = {0903-1936},
  doi       = {10.1183/09031936.00186911},
  pages     = {1458 -- 1467},
  year      = {2012},
  abstract  = {The majority of cases of community-acquired pneumonia are caused by Streptococcus pneumoniae and most studies on pneumococcal host interaction are based on cell culture or animal experiments. Thus, little is known about infections in human lung tissue. Cyclooxygenase-2 and its metabolites play an important regulatory role in lung inflammation. Therefore, we established a pneumococcal infection model on human lung tissue demonstrating mitogen-activated protein kinase (MAPK)-dependent induction of cyclooxygenase-2 and its related metabolites. In addition to alveolar macrophages and the vascular endothelium, cyclooxygenase-2 was upregulated in alveolar type II but not type I epithelial cells, which was confirmed in lungs of patients suffering from acute pneumonia. Moreover, we demonstrated the expression profile of all four E prostanoid receptors at the mRNA level and showed functionality of the E prostanoid(4) receptor by cyclic adenosine monophosphate production. Additionally, in comparison to previous studies, cyclooxygenase-2/prostaglandin E-2 related pro- and anti-inflammatory mediator regulation was partly confirmed in human lung tissue after pneumococcal infection. Overall, cell type-specific and MAPK-dependent cyclooxygenase-2 expression and prostaglandin E-2 formation in human lung tissue may play an important role in the early phase of pneumococcal infections.},
  language  = {en}
}
@article{WallmeyerDietertSochorovaetal.2017,
  author    = {Wallmeyer, Leonie and Dietert, Kristina and Sochorova, Michaela and Gruber, Achim D. and Kleuser, Burkhard and Vavrova, Katerina and Hedtrich, Sarah},
  title     = {TSLP is a direct trigger for T cell migration in filaggrin-deficient skin equivalents},
  series = {Scientific reports},
  volume    = {7},
  journal   = {Scientific reports},
  publisher = {Nature Publ. Group},
  address   = {London},
  issn      = {2045-2322},
  doi       = {10.1038/s41598-017-00670-2},
  pages     = {12},
  year      = {2017},
  abstract  = {Mutations in the gene encoding for filaggrin (FLG) are major predisposing factors for atopic dermatitis (AD). Besides genetic predisposition, immunological dysregulations considerably contribute to its pathophysiology. For example, thymic stromal lymphopoietin (TSLP) is highly expressed in lesional atopic skin and significantly contributes to the pathogenesis of AD by activating dendritic cells that then initiate downstream effects on, for example, T cells. However, little is known about the direct interplay between TSLP, filaggrin-deficient skin and other immune cells such as T lymphocytes. In the present study, FLG knockdown skin equivalents, characterised by intrinsically high TSLP levels, were exposed to activated CD4(+) T cells. T cell exposure resulted in an inflammatory phenotype of the skin equivalents. Furthermore, a distinct shift from a Th1/Th17 to a Th2/Th22 profile was observed following exposure of T cells to filaggrin-deficient skin equivalents. Interestingly, TSLP directly stimulated T cell migration exclusively in filaggrin-deficient skin equivalents even in the absence of dendritic cells, indicating a hitherto unknown role of TSLP in the pathogenesis of AD.},
  language  = {en}
}