@article{BurnsGoldsteinNewgreenetal.2016,
  author    = {Burns, Alan J. and Goldstein, Allan M. and Newgreen, Donald F. and Stamp, Lincon and Sch{\"a}fer, Karl-Herbert and Metzger, Marco and Hotta, Ryo and Young, Heather M. and Andrews, Peter W. and Thapar, Nikhil and Belkind-Gerson, Jaime and Bondurand, Nadege and Bornstein, Joel C. and Chan, Wood Yee and Cheah, Kathryn and Gershon, Michael D. and Heuckeroth, Robert O. and Hofstra, Robert M.W. and Just, Lothar and Kapur, Raj P. and King, Sebastian K. and McCann, Conor J. and Nagy, Nandor and Ngan, Elly and Obermayr, Florian and Pachnis, Vassilis and Pasricha, Pankaj J. and Sham, Mai Har and Tam, Paul and Vanden Berghe, Pieter},
  title     = {White paper on guidelines concerning enteric nervous system stem cell therapy for enteric neuropathies},
  series = {Developmental Biology},
  volume    = {417},
  journal   = {Developmental Biology},
  number    = {2},
  doi       = {10.1016/j.ydbio.2016.04.001},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-187415},
  pages     = {229-251},
  year      = {2016},
  abstract  = {Over the last 20 years, there has been increasing focus on the development of novel stem cell based therapies for the treatment of disorders and diseases affecting the enteric nervous system (ENS) of the gastrointestinal tract (so-called enteric neuropathies). Here, the idea is that ENS progenitor/stem cells could be transplanted into the gut wall to replace the damaged or absent neurons and glia of the ENS. This White Paper sets out experts' views on the commonly used methods and approaches to identify, isolate, purify, expand and optimize ENS stem cells, transplant them into the bowel, and assess transplant success, including restoration of gut function. We also highlight obstacles that must be overcome in order to progress from successful preclinical studies in animal models to ENS stem cell therapies in the clinic.},
  language  = {en}
}
@article{WoersdoerferDaldaKernetal.2019,
  author    = {W{\"o}rsd{\"o}rfer, Philipp and Dalda, Nahide and Kern, Anna and Kr{\"u}ger, Sarah and Wagner, Nicole and Kwok, Chee Keong and Henke, Erik and Erg{\"u}n, S{\"u}leyman},
  title     = {Generation of complex human organoid models including vascular networks by incorporation of mesodermal progenitor cells},
  series = {Scientific Reports},
  volume    = {9},
  journal   = {Scientific Reports},
  doi       = {10.1038/s41598-019-52204-7},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-202681},
  pages     = {15663},
  year      = {2019},
  abstract  = {Organoids derived from human pluripotent stem cells are interesting models to study mechanisms of morphogenesis and promising platforms for disease modeling and drug screening. However, they mostly remain incomplete as they lack stroma, tissue resident immune cells and in particular vasculature, which create important niches during development and disease. We propose, that the directed incorporation of mesodermal progenitor cells (MPCs) into organoids will overcome the aforementioned limitations. In order to demonstrate the feasibility of the method, we generated complex human tumor as well as neural organoids. We show that the formed blood vessels display a hierarchic organization and mural cells are assembled into the vessel wall. Moreover, we demonstrate a typical blood vessel ultrastructure including endothelial cell-cell junctions, a basement membrane as well as luminal caveolae and microvesicles. We observe a high plasticity in the endothelial network, which expands, while the organoids grow and is responsive to anti-angiogenic compounds and pro-angiogenic conditions such as hypoxia. We show that vessels within tumor organoids connect to host vessels following transplantation. Remarkably, MPCs also deliver Iba1\(^+\) cells that infiltrate the neural tissue in a microglia-like manner.},
  language  = {en}
}
@article{KimMcDonaghDengetal.2019,
  author    = {Kim, Brandon J. and McDonagh, Maura A. and Deng, Liwen and Gastfriend, Benjamin D. and Schubert-Unkmeir, Alexandra and Doran, Kelly S. and Shusta, Eric V.},
  title     = {Streptococcus agalactiae disrupts P-glycoprotein function in brain endothelial cells},
  series = {Fluids and Barriers of the CNS},
  volume    = {16},
  journal   = {Fluids and Barriers of the CNS},
  doi       = {10.1186/s12987-019-0146-5},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-201895},
  pages     = {26},
  year      = {2019},
  abstract  = {Bacterial meningitis is a serious life threatening infection of the CNS. To cause meningitis, blood-borne bacteria need to interact with and penetrate brain endothelial cells (BECs) that comprise the blood-brain barrier. BECs help maintain brain homeostasis and they possess an array of efflux transporters, such as P-glycoprotein (P-gp), that function to efflux potentially harmful compounds from the CNS back into the circulation. Oftentimes, efflux also serves to limit the brain uptake of therapeutic drugs, representing a major hurdle for CNS drug delivery. During meningitis, BEC barrier integrity is compromised; however, little is known about efflux transport perturbations during infection. Thus, understanding the impact of bacterial infection on P-gp function would be important for potential routes of therapeutic intervention. To this end, the meningeal bacterial pathogen, Streptococcus agalactiae, was found to inhibit P-gp activity in human induced pluripotent stem cell-derived BECs, and live bacteria were required for the observed inhibition. This observation was correlated to decreased P-gp expression both in vitro and during infection in vivo using a mouse model of bacterial meningitis. Given the impact of bacterial interactions on P-gp function, it will be important to incorporate these findings into analyses of drug delivery paradigms for bacterial infections of the CNS.},
  language  = {en}
}