Sandra Jagdmann
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Sandra Jagdmann has a total of 8 co-authors. Here are the top co-authors by number of shared publications:
- Andreas Meisel
Department of Neurology with Experimental Neurology, Charité – University Medical Center Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany
2 shared publications - Christian Meisel
Department of Immunology, Labor Berlin Charité-Vivantes , Berlin
2 shared publications - Claudia Dames
Department of Neurology with Experimental Neurology, Center for Stroke Research Berlin, Charité–Universitätsmedizin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Germany (C.D., D.B., A.M.).
2 shared publications - Daniel Berchtold
Department of Neurology with Experimental Neurology, Center for Stroke Research Berlin, Charité - Universitätsmedizin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin, Germany
2 shared publications - Birgitt Gutbier
Department of Infectious Diseases and Respiratory Medicine, Charité—Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany
1 shared publication - Katarzyna Winek
Leibniz Institute on Aging, Fritz Lipmann Institute (FLI), Jena, Germany
1 shared publication
Latest Publications
- Open Access
- 1 June 2021
- Published by Elsevier in Journal of Neuroimmunology
- Vol. 355, 577568
Efficacy and safety of intratracheal IFN-γ treatment to reverse stroke-induced susceptibility to pulmonary bacterial infections
- 1 June 2021
- Published by Elsevier in Journal of Neuroimmunology
- Vol. 355, 577568
Open AccessEfficacy and safety of intratracheal IFN-γ treatment to reverse stroke-induced susceptibility to pulmonary bacterial infections
- Open Access
Impact of Key Nicotinic AChR Subunits on Post-Stroke Pneumococcal Pneumonia
Pneumonia is the most frequent severe medical complication after stroke. An overactivation of the cholinergic signaling after stroke contributes to immunosuppression and the development of spontaneous pneumonia caused by Gram-negative pathogens. The α7 nicotinic acetylcholine receptor (α7nAChR) has already been identified as an important mediator of the anti-inflammatory pathway after stroke. However, whether the α2, α5 and α9/10 nAChR expressed in the lung also play a role in suppression of pulmonary innate immunity after stroke is unknown. In the present study, we investigate the impact of various nAChRs on aspiration-induced pneumonia after stroke. Therefore, α2, α5, α7 and α9/10 nAChR knockout (KO) mice and wild type (WT) littermates were infected with Streptococcus pneumoniae (S. pneumoniae) three days after middle cerebral artery occlusion (MCAo). One day after infection pathogen clearance, cellularity in lung and spleen, cytokine secretion in bronchoalveolar lavage (BAL) and alveolar-capillary barrier were investigated. Here, we found that deficiency of various nAChRs does not contribute to an enhanced clearance of a Gram-positive pathogen causing post-stroke pneumonia in mice. In conclusion, these findings suggest that a single nAChR is not sufficient to mediate the impaired pulmonary defense against S. pneumoniae after experimental stroke.
Open AccessImpact of Key Nicotinic AChR Subunits on Post-Stroke Pneumococcal Pneumonia
Pneumonia is the most frequent severe medical complication after stroke. An overactivation of the cholinergic signaling after stroke contributes to immunosuppression and the development of spontaneous pneumonia caused by Gram-negative pathogens. The α7 nicotinic acetylcholine receptor (α7nAChR) has already been identified as an important mediator of the anti-inflammatory pathway after stroke. However, whether the α2, α5 and α9/10 nAChR expressed in the lung also play a role in suppression of pulmonary innate immunity after stroke is unknown. In the present study, we investigate the impact of various nAChRs on aspiration-induced pneumonia after stroke. Therefore, α2, α5, α7 and α9/10 nAChR knockout (KO) mice and wild type (WT) littermates were infected with Streptococcus pneumoniae (S. pneumoniae) three days after middle cerebral artery occlusion (MCAo). One day after infection pathogen clearance, cellularity in lung and spleen, cytokine secretion in bronchoalveolar lavage (BAL) and alveolar-capillary barrier were investigated. Here, we found that deficiency of various nAChRs does not contribute to an enhanced clearance of a Gram-positive pathogen causing post-stroke pneumonia in mice. In conclusion, these findings suggest that a single nAChR is not sufficient to mediate the impaired pulmonary defense against S. pneumoniae after experimental stroke.