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...
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| Format: | Article |
| Language: | English |
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MDPI AG
2020-05-01
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| Series: | Vaccines |
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| Online Access: | https://www.mdpi.com/2076-393X/8/2/253 |
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| author | Sandra Jagdmann Claudia Dames Daniel Berchtold Katarzyna Winek Luis Weitbrecht Andreas Meisel Christian Meisel |
| author_facet | Sandra Jagdmann Claudia Dames Daniel Berchtold Katarzyna Winek Luis Weitbrecht Andreas Meisel Christian Meisel |
| author_sort | Sandra Jagdmann |
| collection | DOAJ |
| description | 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 <i>Streptococcus pneumoniae</i> (<i>S. pneumoniae</i>) 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 <i>S. pneumoniae</i> after experimental stroke. |
| first_indexed | 2024-03-10T19:32:57Z |
| format | Article |
| id | doaj.art-ac0282bfd45d443ba2217f4ac9b11d7e |
| institution | Directory Open Access Journal |
| issn | 2076-393X |
| language | English |
| last_indexed | 2024-03-10T19:32:57Z |
| publishDate | 2020-05-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Vaccines |
| spelling | doaj.art-ac0282bfd45d443ba2217f4ac9b11d7e2023-11-20T01:59:21ZengMDPI AGVaccines2076-393X2020-05-018225310.3390/vaccines8020253Impact of Key Nicotinic AChR Subunits on Post-Stroke Pneumococcal PneumoniaSandra Jagdmann0Claudia Dames1Daniel Berchtold2Katarzyna Winek3Luis Weitbrecht4Andreas Meisel5Christian Meisel6Institute for Medical Immunology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, 13353 Berlin, GermanyInstitute for Medical Immunology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, 13353 Berlin, GermanyDepartment of Experimental Neurology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, 10117 Berlin, GermanyDepartment of Experimental Neurology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, 10117 Berlin, GermanyDepartment of Experimental Neurology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, 10117 Berlin, GermanyDepartment of Experimental Neurology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, 10117 Berlin, GermanyInstitute for Medical Immunology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, 13353 Berlin, GermanyPneumonia 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 <i>Streptococcus pneumoniae</i> (<i>S. pneumoniae</i>) 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 <i>S. pneumoniae</i> after experimental stroke.https://www.mdpi.com/2076-393X/8/2/253MCAoimmunosuppressionnicotinic acetylcholine receptoraspiration-induced pneumonia<i>Streptococcus pneumoniae</i> |
| spellingShingle | Sandra Jagdmann Claudia Dames Daniel Berchtold Katarzyna Winek Luis Weitbrecht Andreas Meisel Christian Meisel Impact of Key Nicotinic AChR Subunits on Post-Stroke Pneumococcal Pneumonia Vaccines MCAo immunosuppression nicotinic acetylcholine receptor aspiration-induced pneumonia <i>Streptococcus pneumoniae</i> |
| title | Impact of Key Nicotinic AChR Subunits on Post-Stroke Pneumococcal Pneumonia |
| title_full | Impact of Key Nicotinic AChR Subunits on Post-Stroke Pneumococcal Pneumonia |
| title_fullStr | Impact of Key Nicotinic AChR Subunits on Post-Stroke Pneumococcal Pneumonia |
| title_full_unstemmed | Impact of Key Nicotinic AChR Subunits on Post-Stroke Pneumococcal Pneumonia |
| title_short | Impact of Key Nicotinic AChR Subunits on Post-Stroke Pneumococcal Pneumonia |
| title_sort | impact of key nicotinic achr subunits on post stroke pneumococcal pneumonia |
| topic | MCAo immunosuppression nicotinic acetylcholine receptor aspiration-induced pneumonia <i>Streptococcus pneumoniae</i> |
| url | https://www.mdpi.com/2076-393X/8/2/253 |
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