Vagus nerve inflammation contributes to dysautonomia in COVID-19
Dysautonomia has substantially impacted acute COVID-19 severity as well as symptom burden after recovery from COVID-19 (long COVID), yet the underlying causes remain unknown. Here, we hypothesized that vagus nerves are affected in COVID-19 which might contribute to autonomic dysfunction. We performe...
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| Veröffentlicht in: | Acta neuropathologica 2023-09, Vol.146 (3), p.387-394 |
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| creator | Woo, Marcel S. Shafiq, Mohsin Fitzek, Antonia Dottermusch, Matthias Altmeppen, Hermann Mohammadi, Behnam Mayer, Christina Bal, Lukas C. Raich, Lukas Matschke, Jakob Krasemann, Susanne Pfefferle, Susanne Brehm, Thomas Theo Lütgehetmann, Marc Schädler, Julia Addo, Marylyn M. Schulze zur Wiesch, Julian Ondruschka, Benjamin Friese, Manuel A. Glatzel, Markus |
| description | Dysautonomia has substantially impacted acute COVID-19 severity as well as symptom burden after recovery from COVID-19 (long COVID), yet the underlying causes remain unknown. Here, we hypothesized that vagus nerves are affected in COVID-19 which might contribute to autonomic dysfunction. We performed a histopathological characterization of
postmortem
vagus nerves from COVID-19 patients and controls, and detected SARS-CoV-2 RNA together with inflammatory cell infiltration composed primarily of monocytes. Furthermore, we performed RNA sequencing which revealed a strong inflammatory response of neurons, endothelial cells, and Schwann cells which correlated with SARS-CoV-2 RNA load. Lastly, we screened a clinical cohort of 323 patients to detect a clinical phenotype of vagus nerve affection and found a decreased respiratory rate in non-survivors of critical COVID-19. Our data suggest that SARS-CoV-2 induces vagus nerve inflammation followed by autonomic dysfunction which contributes to critical disease courses and might contribute to dysautonomia observed in long COVID. |
| doi_str_mv | 10.1007/s00401-023-02612-x |
| format | Article |
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postmortem
vagus nerves from COVID-19 patients and controls, and detected SARS-CoV-2 RNA together with inflammatory cell infiltration composed primarily of monocytes. Furthermore, we performed RNA sequencing which revealed a strong inflammatory response of neurons, endothelial cells, and Schwann cells which correlated with SARS-CoV-2 RNA load. Lastly, we screened a clinical cohort of 323 patients to detect a clinical phenotype of vagus nerve affection and found a decreased respiratory rate in non-survivors of critical COVID-19. Our data suggest that SARS-CoV-2 induces vagus nerve inflammation followed by autonomic dysfunction which contributes to critical disease courses and might contribute to dysautonomia observed in long COVID.</description><identifier>ISSN: 0001-6322</identifier><identifier>EISSN: 1432-0533</identifier><identifier>DOI: 10.1007/s00401-023-02612-x</identifier><identifier>PMID: 37452829</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Autonomic nervous system ; Cloning ; COVID-19 ; Disease ; Dysautonomia ; Endothelial cells ; Generalized linear models ; Genes ; Health aspects ; Inflammation ; Legal medicine ; Long COVID ; Medicine ; Medicine & Public Health ; Monocytes ; Neurosciences ; Original Paper ; Pathology ; Phenotypes ; Respiration ; Ribonucleic acid ; RNA ; RNA sequencing ; Schwann cells ; Severe acute respiratory syndrome coronavirus 2 ; Vagus nerve</subject><ispartof>Acta neuropathologica, 2023-09, Vol.146 (3), p.387-394</ispartof><rights>The Author(s) 2023</rights><rights>2023. The Author(s).</rights><rights>COPYRIGHT 2023 Springer</rights><rights>The Author(s) 2023. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c542t-48d2082b42dd77a65e42f500a453cb87e0a89a4c129c1d46bf7e82671279eeab3</citedby><cites>FETCH-LOGICAL-c542t-48d2082b42dd77a65e42f500a453cb87e0a89a4c129c1d46bf7e82671279eeab3</cites><orcidid>0000-0002-1306-2708 ; 0000-0002-7720-8817 ; 0000-0002-9468-7944 ; 0000-0002-9178-3949 ; 0000-0002-4148-2822 ; 0000-0003-2836-9224 ; 0000-0003-4731-2311 ; 0000-0001-6380-2420</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00401-023-02612-x$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00401-023-02612-x$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,27903,27904,41467,42536,51298</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37452829$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Woo, Marcel S.</creatorcontrib><creatorcontrib>Shafiq, Mohsin</creatorcontrib><creatorcontrib>Fitzek, Antonia</creatorcontrib><creatorcontrib>Dottermusch, Matthias</creatorcontrib><creatorcontrib>Altmeppen, Hermann</creatorcontrib><creatorcontrib>Mohammadi, Behnam</creatorcontrib><creatorcontrib>Mayer, Christina</creatorcontrib><creatorcontrib>Bal, Lukas C.</creatorcontrib><creatorcontrib>Raich, Lukas</creatorcontrib><creatorcontrib>Matschke, Jakob</creatorcontrib><creatorcontrib>Krasemann, Susanne</creatorcontrib><creatorcontrib>Pfefferle, Susanne</creatorcontrib><creatorcontrib>Brehm, Thomas Theo</creatorcontrib><creatorcontrib>Lütgehetmann, Marc</creatorcontrib><creatorcontrib>Schädler, Julia</creatorcontrib><creatorcontrib>Addo, Marylyn M.</creatorcontrib><creatorcontrib>Schulze zur Wiesch, Julian</creatorcontrib><creatorcontrib>Ondruschka, Benjamin</creatorcontrib><creatorcontrib>Friese, Manuel A.</creatorcontrib><creatorcontrib>Glatzel, Markus</creatorcontrib><title>Vagus nerve inflammation contributes to dysautonomia in COVID-19</title><title>Acta neuropathologica</title><addtitle>Acta Neuropathol</addtitle><addtitle>Acta Neuropathol</addtitle><description>Dysautonomia has substantially impacted acute COVID-19 severity as well as symptom burden after recovery from COVID-19 (long COVID), yet the underlying causes remain unknown. Here, we hypothesized that vagus nerves are affected in COVID-19 which might contribute to autonomic dysfunction. We performed a histopathological characterization of
postmortem
vagus nerves from COVID-19 patients and controls, and detected SARS-CoV-2 RNA together with inflammatory cell infiltration composed primarily of monocytes. Furthermore, we performed RNA sequencing which revealed a strong inflammatory response of neurons, endothelial cells, and Schwann cells which correlated with SARS-CoV-2 RNA load. Lastly, we screened a clinical cohort of 323 patients to detect a clinical phenotype of vagus nerve affection and found a decreased respiratory rate in non-survivors of critical COVID-19. Our data suggest that SARS-CoV-2 induces vagus nerve inflammation followed by autonomic dysfunction which contributes to critical disease courses and might contribute to dysautonomia observed in long COVID.</description><subject>Autonomic nervous system</subject><subject>Cloning</subject><subject>COVID-19</subject><subject>Disease</subject><subject>Dysautonomia</subject><subject>Endothelial cells</subject><subject>Generalized linear models</subject><subject>Genes</subject><subject>Health aspects</subject><subject>Inflammation</subject><subject>Legal medicine</subject><subject>Long COVID</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Monocytes</subject><subject>Neurosciences</subject><subject>Original Paper</subject><subject>Pathology</subject><subject>Phenotypes</subject><subject>Respiration</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA sequencing</subject><subject>Schwann cells</subject><subject>Severe acute 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postmortem
vagus nerves from COVID-19 patients and controls, and detected SARS-CoV-2 RNA together with inflammatory cell infiltration composed primarily of monocytes. Furthermore, we performed RNA sequencing which revealed a strong inflammatory response of neurons, endothelial cells, and Schwann cells which correlated with SARS-CoV-2 RNA load. Lastly, we screened a clinical cohort of 323 patients to detect a clinical phenotype of vagus nerve affection and found a decreased respiratory rate in non-survivors of critical COVID-19. Our data suggest that SARS-CoV-2 induces vagus nerve inflammation followed by autonomic dysfunction which contributes to critical disease courses and might contribute to dysautonomia observed in long COVID.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>37452829</pmid><doi>10.1007/s00401-023-02612-x</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-1306-2708</orcidid><orcidid>https://orcid.org/0000-0002-7720-8817</orcidid><orcidid>https://orcid.org/0000-0002-9468-7944</orcidid><orcidid>https://orcid.org/0000-0002-9178-3949</orcidid><orcidid>https://orcid.org/0000-0002-4148-2822</orcidid><orcidid>https://orcid.org/0000-0003-2836-9224</orcidid><orcidid>https://orcid.org/0000-0003-4731-2311</orcidid><orcidid>https://orcid.org/0000-0001-6380-2420</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Acta neuropathologica, 2023-09, Vol.146 (3), p.387-394 |
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| language | eng |
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| source | Springer Nature - Complete Springer Journals |
| subjects | Autonomic nervous system Cloning COVID-19 Disease Dysautonomia Endothelial cells Generalized linear models Genes Health aspects Inflammation Legal medicine Long COVID Medicine Medicine & Public Health Monocytes Neurosciences Original Paper Pathology Phenotypes Respiration Ribonucleic acid RNA RNA sequencing Schwann cells Severe acute respiratory syndrome coronavirus 2 Vagus nerve |
| title | Vagus nerve inflammation contributes to dysautonomia in COVID-19 |
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