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Open AccessArticle

Impact of Key Nicotinic AChR Subunits on Post-Stroke Pneumococcal Pneumonia

1
Institute for Medical Immunology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, 13353 Berlin, Germany
2
Department of Experimental Neurology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, 10117 Berlin, Germany
3
Center for Stroke Research Berlin, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 10117 Berlin, Germany
4
Neurocure Clinical Research Center, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 10117 Berlin, Germany
5
Department of Neurology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 10117 Berlin, Germany
6
Labor Berlin, Charité-Universitätsmedizin Berlin Vivantes, 10117 Berlin, Germany
*
Author to whom correspondence should be addressed.
Vaccines 2020, 8(2), 253; https://doi.org/10.3390/vaccines8020253
Received: 30 April 2020 / Revised: 25 May 2020 / Accepted: 25 May 2020 / Published: 28 May 2020
(This article belongs to the Special Issue Research on Innate Immunity and Inflammation)
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. View Full-Text
Keywords: MCAo; immunosuppression; nicotinic acetylcholine receptor; aspiration-induced pneumonia; Streptococcus pneumoniae MCAo; immunosuppression; nicotinic acetylcholine receptor; aspiration-induced pneumonia; Streptococcus pneumoniae
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Jagdmann, S.; Dames, C.; Berchtold, D.; Winek, K.; Weitbrecht, L.; Meisel, A.; Meisel, C. Impact of Key Nicotinic AChR Subunits on Post-Stroke Pneumococcal Pneumonia. Vaccines 2020, 8, 253.

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