@article{RadbruchPischonOstrowskietal.2017,
  author    = {Radbruch, Moritz and Pischon, Hannah and Ostrowski, Anja and Volz, Pierre and Brodwolf, Robert and Neumann, Falko and Unbehauen, Michael and Kleuser, Burkhard and Haag, Rainer and Ma, Nan and Alexiev, Ulrike and Mundhenk, Lars and Gruber, Achim D.},
  title     = {Dendritic core-multishell nanocarriers in murine models of healthy and atopic skin},
  series = {Nanoscale Research Letters},
  volume    = {12},
  journal   = {Nanoscale Research Letters},
  number    = {64},
  publisher = {Springer},
  address   = {New York},
  issn      = {1556-276X},
  doi       = {10.1186/s11671-017-1835-0},
  pages     = {12},
  year      = {2017},
  abstract  = {Dendritic hPG-amid-C18-mPEG core-multishell nanocarriers (CMS) represent a novel class of unimolecular micelles that hold great potential as drug transporters, e. g., to facilitate topical therapy in skin diseases. Atopic dermatitis is among the most common inflammatory skin disorders with complex barrier alterations which may affect the efficacy of topical treatment. Here, we tested the penetration behavior and identified target structures of unloaded CMS after topical administration in healthy mice and in mice with oxazolone-induced atopic dermatitis. We further examined whole body distribution and possible systemic side effects after simulating high dosage dermal penetration by subcutaneous injection. Following topical administration, CMS accumulated in the stratum corneum without penetration into deeper viable epidermal layers. The same was observed in atopic dermatitis mice, indicating that barrier alterations in atopic dermatitis had no influence on the penetration of CMS. Following subcutaneous injection, CMS were deposited in the regional lymph nodes as well as in liver, spleen, lung, and kidney. However, in vitro toxicity tests, clinical data, and morphometry-assisted histopathological analyses yielded no evidence of any toxic or otherwise adverse local or systemic effects of CMS, nor did they affect the severity or course of atopic dermatitis. Taken together, CMS accumulate in the stratum corneum in both healthy and inflammatory skin and appear to be highly biocompatible in the mouse even under conditions of atopic dermatitis and thus could potentially serve to create a depot for anti-inflammatory drugs in the skin.},
  language  = {en}
}
@misc{RadbruchPischonOstrowskietal.2017,
  author    = {Radbruch, Moritz and Pischon, Hannah and Ostrowski, Anja and Volz, Pierre and Brodwolf, Robert and Neumann, Falko and Unbehauen, Michael and Kleuser, Burkhard and Haag, Rainer and Ma, Nan and Alexiev, Ulrike and Mundhenk, Lars and Gruber, Achim D.},
  title     = {Dendritic core-multishell nanocarriers in murine models of healthy and atopic skin},
  series = {Postprints der Universit{\"a}t Potsdam Mathematisch-Naturwissenschaftliche Reihe},
  journal   = {Postprints der Universit{\"a}t Potsdam Mathematisch-Naturwissenschaftliche Reihe},
  number    = {724},
  issn      = {1866-8372},
  doi       = {10.25932/publishup-43013},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-430136},
  pages     = {12},
  year      = {2017},
  abstract  = {Dendritic hPG-amid-C18-mPEG core-multishell nanocarriers (CMS) represent a novel class of unimolecular micelles that hold great potential as drug transporters, e. g., to facilitate topical therapy in skin diseases. Atopic dermatitis is among the most common inflammatory skin disorders with complex barrier alterations which may affect the efficacy of topical treatment. Here, we tested the penetration behavior and identified target structures of unloaded CMS after topical administration in healthy mice and in mice with oxazolone-induced atopic dermatitis. We further examined whole body distribution and possible systemic side effects after simulating high dosage dermal penetration by subcutaneous injection. Following topical administration, CMS accumulated in the stratum corneum without penetration into deeper viable epidermal layers. The same was observed in atopic dermatitis mice, indicating that barrier alterations in atopic dermatitis had no influence on the penetration of CMS. Following subcutaneous injection, CMS were deposited in the regional lymph nodes as well as in liver, spleen, lung, and kidney. However, in vitro toxicity tests, clinical data, and morphometry-assisted histopathological analyses yielded no evidence of any toxic or otherwise adverse local or systemic effects of CMS, nor did they affect the severity or course of atopic dermatitis. Taken together, CMS accumulate in the stratum corneum in both healthy and inflammatory skin and appear to be highly biocompatible in the mouse even under conditions of atopic dermatitis and thus could potentially serve to create a depot for anti-inflammatory drugs in the skin.},
  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{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}
}