Sandra Manthey
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Sandra Manthey has a total of 10 co-authors. Here are the top co-authors by number of shared publications:
- Arndt Vogel
Division of Gastroenterology and Hepatology, Toronto General Hospital, Medical Oncology, Princess Margaret Cancer Centre, University of Toronto, Canada
1 shared publication - Aurora De Ponti
Division of Signal Transduction and Growth Control, DKFZ-ZMBH Alliance, German Cancer Research Center (DKFZ), Heidelberg, Germany
1 shared publication - Christine Bauer
Division of Signal Transduction and Growth Control, DKFZ-ZMBH Alliance, German Cancer Research Center (DKFZ), Heidelberg, Germany
1 shared publication - Jochen Hess
Department of Otorhinolaryngology, Head and Neck Surgery University Hospital Heidelberg Heidelberg Germany
1 shared publication - Julia Németh
Division of Signal Transduction and Growth Control, DKFZ-ZMBH Alliance, German Cancer Research Center (DKFZ), Heidelberg, Germany
1 shared publication - Lars Wiechert
Division of Signal Transduction and Growth Control, DKFZ-ZMBH Alliance, German Cancer Research Center (DKFZ), Heidelberg, Germany
1 shared publication
Latest Publications
- Open Access
- 15 December 2012
- Published by Springer Nature in Cell Communication and Signaling
- Vol. 10 (1) , 40
Hepatocyte-specific S100a8 and S100a9 transgene expression in mice causes Cxcl1 induction and systemic neutrophil enrichment
Background: Calprotectin consists of the Ca2+-binding proteins S100a8 and S100a9 that are induced in epithelial cells in response to tissue damage and infection. Both proteins are also secreted by activated innate immune cells and numerous studies demonstrate their crucial role in pathological conditions of acute and chronic inflammation.Results: Here, we established a conditional mouse model with simultaneousS100a8andS100a9transgene expression in hepatocytes (TgS100a8a9hep) under the control of doxycycline to unravel the role of epithelial-derived Calprotectin on tissue homeostasis and inflammation.TgS100a8a9hepmice displayed a significant enrichment of neutrophils in peripheral blood and tissues with high blood content. Interestingly,Cxcl1transcription was significantly induced in the liver ofTgS100a8a9hepmice and primary hepatocytes derived thereof as compared to Control mice, accompanied by an increase of Cxcl1 serum levels. However, expression of other chemokines with a known function in neutrophil mobilization from the bone marrow, e.g. Csf3 and Cxcl2, was not altered. Doxycycline treatment ofTgS100a8a9hepmice reducedCxcl1expression in the liver and resulted in normal numbers of neutrophils.Conclusion: In summary, our data demonstrate for the first time that hepatocyte-specific S100a8 and S100a9 expression induces a systemic mobilization of neutrophils by a specific activation of Cxcl1 transcription in the liver.
- 15 December 2012
- Published by Springer Nature in Cell Communication and Signaling
- Vol. 10 (1) , 40
Open AccessHepatocyte-specific S100a8 and S100a9 transgene expression in mice causes Cxcl1 induction and systemic neutrophil enrichment
Background: Calprotectin consists of the Ca2+-binding proteins S100a8 and S100a9 that are induced in epithelial cells in response to tissue damage and infection. Both proteins are also secreted by activated innate immune cells and numerous studies demonstrate their crucial role in pathological conditions of acute and chronic inflammation.Results: Here, we established a conditional mouse model with simultaneousS100a8andS100a9transgene expression in hepatocytes (TgS100a8a9hep) under the control of doxycycline to unravel the role of epithelial-derived Calprotectin on tissue homeostasis and inflammation.TgS100a8a9hepmice displayed a significant enrichment of neutrophils in peripheral blood and tissues with high blood content. Interestingly,Cxcl1transcription was significantly induced in the liver ofTgS100a8a9hepmice and primary hepatocytes derived thereof as compared to Control mice, accompanied by an increase of Cxcl1 serum levels. However, expression of other chemokines with a known function in neutrophil mobilization from the bone marrow, e.g. Csf3 and Cxcl2, was not altered. Doxycycline treatment ofTgS100a8a9hepmice reducedCxcl1expression in the liver and resulted in normal numbers of neutrophils.Conclusion: In summary, our data demonstrate for the first time that hepatocyte-specific S100a8 and S100a9 expression induces a systemic mobilization of neutrophils by a specific activation of Cxcl1 transcription in the liver.