Vagus nerve inflammation contributes to dysautonomia in COVID-19

Standard

Harvard

APA

Vancouver

Bibtex

@article{8e09cf96301b4158b76b43ce9d7362a6,
title = "Vagus nerve inflammation contributes to dysautonomia in COVID-19",
abstract = "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.",
author = "Woo, {Marcel S} and Mohsin Shafiq and Antonia Fitzek and Matthias Dottermusch and Hermann Altmeppen and Behnam Mohammadi and Christina Mayer and Bal, {Lukas C} and Lukas Raich and Jakob Matschke and Susanne Krasemann and Susanne Pfefferle and Brehm, {Thomas Theo} and Marc L{\"u}tgehetmann and Julia Sch{\"a}dler and Addo, {Marylyn M} and {Schulze Zur Wiesch}, Julian and Benjamin Ondruschka and Friese, {Manuel A} and Markus Glatzel",
note = "{\textcopyright} 2023. The Author(s).",
year = "2023",
month = sep,
doi = "10.1007/s00401-023-02612-x",
language = "English",
volume = "146",
pages = "387--394",
journal = "ACTA NEUROPATHOL",
issn = "0001-6322",
publisher = "Springer",
number = "3",

}

RIS

TY - JOUR

T1 - Vagus nerve inflammation contributes to dysautonomia in COVID-19

AU - Woo, Marcel S

AU - Shafiq, Mohsin

AU - Fitzek, Antonia

AU - Dottermusch, Matthias

AU - Altmeppen, Hermann

AU - Mohammadi, Behnam

AU - Mayer, Christina

AU - Bal, Lukas C

AU - Raich, Lukas

AU - Matschke, Jakob

AU - Krasemann, Susanne

AU - Pfefferle, Susanne

AU - Brehm, Thomas Theo

AU - Lütgehetmann, Marc

AU - Schädler, Julia

AU - Addo, Marylyn M

AU - Schulze Zur Wiesch, Julian

AU - Ondruschka, Benjamin

AU - Friese, Manuel A

AU - Glatzel, Markus

N1 - © 2023. The Author(s).

PY - 2023/9

Y1 - 2023/9

N2 - 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.

AB - 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.

U2 - 10.1007/s00401-023-02612-x

DO - 10.1007/s00401-023-02612-x

M3 - SCORING: Journal article

C2 - 37452829

VL - 146

SP - 387

EP - 394

JO - ACTA NEUROPATHOL

JF - ACTA NEUROPATHOL

SN - 0001-6322

IS - 3

ER -