Luis Weitbrecht
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Luis Weitbrecht has a total of 6 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
1 shared publication - Christian Meisel
Department of Immunology, Labor Berlin Charité-Vivantes , Berlin
1 shared publication - 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.).
1 shared publication - 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
1 shared publication - Katarzyna Winek
Leibniz Institute on Aging, Fritz Lipmann Institute (FLI), Jena, Germany
1 shared publication - Sandra Jagdmann
Charite, Augustenburger Pl 1, D-13353 Berlin, Germany
1 shared publication
Latest Publications
- 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.