@article{CzakaiLeonhardtDixetal.2016,
  author    = {Czakai, Kristin and Leonhardt, Ines and Dix, Andreas and Bonin, Michael and Linde, Joerg and Einsele, Hermann and Kurzai, Oliver and Loeffler, J{\"u}rgen},
  title     = {Kr{\"u}ppel-like Factor 4 modulates interleukin-6 release in human dendritic cells after in vitro stimulation with Aspergillus fumigatus and Candida albicans},
  series = {Scientific Reports},
  volume    = {6},
  journal   = {Scientific Reports},
  doi       = {10.1038/srep27990},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-181185},
  year      = {2016},
  abstract  = {Invasive fungal infections are associated with high mortality rates and are mostly caused by the opportunistic fungi Aspergillus fumigatus and Candida albicans. Immune responses against these fungi are still not fully understood. Dendritic cells (DCs) are crucial players in initiating innate and adaptive immune responses against fungal infections. The immunomodulatory effects of fungi were compared to the bacterial stimulus LPS to determine key players in the immune response to fungal infections. A genome wide study of the gene regulation of human monocyte-derived dendritic cells (DCs) confronted with A. fumigatus, C. albicans or LPS was performed and Kr{\"u}ppel-like factor 4 (KLF4) was identified as the only transcription factor that was down-regulated in DCs by both fungi but induced by stimulation with LPS. Downstream analysis demonstrated the influence of KLF4 on the interleukine-6 expression in human DCs. Furthermore, KLF4 regulation was shown to be dependent on pattern recognition receptor ligation. Therefore KLF4 was identified as a controlling element in the IL-6 immune response with a unique expression pattern comparing fungal and LPS stimulation.},
  language  = {en}
}
@article{WhiteWiederholdLoeffleretal.2016,
  author    = {White, P. Lewis and Wiederhold, Nathan P. and Loeffler, Juergen and Najvar, Laura K. and Melchers, Willem and Herrera, Monica and Bretagne, Stephane and Wickes, Brian and Kirkpatrick, William R. and Barnes, Rosemary A. and Donnelly, J. Peter and Patterson, Thomas F.},
  title     = {Comparison of nonculture blood-based tests for diagnosing invasive aspergillosis in an animal model},
  series = {Journal of Clinical Microbiology},
  volume    = {54},
  journal   = {Journal of Clinical Microbiology},
  number    = {4},
  doi       = {10.1128/JCM.03233-15},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-189674},
  pages     = {960-966},
  year      = {2016},
  abstract  = {The European Aspergillus PCR Initiative (EAPCRI) has provided recommendations for the PCR testing of whole blood (WB) and serum/plasma. It is important to test these recommended protocols on nonsimulated "in vivo" specimens before full clinical evaluation. The testing of an animal model of invasive aspergillosis (IA) overcomes the low incidence of disease and provides experimental design and control that is not possible in the clinical setting. Inadequate performance of the recommended protocols at this stage would require reassessment of methods before clinical trials are performed and utility assessed. The manuscript describes the performance of EAPCRI protocols in an animal model of invasive aspergillosis. Blood samples taken from a guinea pig model of IA were used for WB and serum PCR. Galactomannan and beta-D-glucan detection were evaluated, with particular focus on the timing of positivity and on the interpretation of combination testing. The overall sensitivities for WB PCR, serum PCR, galactomannan, and beta-D-glucan were 73\%, 65\%, 68\%, and 46\%, respectively. The corresponding specificities were 92\%, 79\%, 80\%, and 100\%, respectively. PCR provided the earliest indicator of IA, and increasing galactomannan and beta-D-glucan values were indicators of disease progression. The combination of WB PCR with galactomannan and beta-D-glucan proved optimal (area under the curve AUC], 0.95), and IA was confidently diagnosed or excluded. The EAPRCI-recommended PCR protocols provide performance comparable to commercial antigen tests, and clinical trials are warranted. By combining multiple tests, IA can be excluded or confirmed, highlighting the need for a combined diagnostic strategy. However, this approach must be balanced against the practicality and cost of using multiple tests.},
  language  = {en}
}