Autonomic balance determines the severity of COVID-19 courses
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Bioelectronic Medicine
HYPOTHESIS
Open Access
Autonomic balance determines the severity of COVID-19 courses M. Leitzke1* , D. Stefanovic1, J.-J. Meyer1, S. Schimpf2 and P. Schönknecht3
Abstract COVID-19 has left mankind desperately seeking how to manage dramatically rising infection rates associated with severe disease progressions. COVID-19 courses range from mild symptoms up to multiple organ failure and death, triggered by excessively high serum cytokine levels (IL 1β, IL 6, TNF α, IL 8). The vagally driven cholinergic anti-inflammatory pathway (CAP) stops the action of nuclear factor κB (NF-κB), the transcriptional factor of pro-inflammatory cytokines. Thus, wellbalanced cytokine release depends on adequate vagal signaling. Coronaviruses replicate using NF-κB transcriptional factor as well. By degrading the cytoplasmatic inhibitor of NF-κB subunits (IκB), coronaviruses induce unrestricted NF-κB expression accelerating both, virus replication and cytokine transcription. We hypothesize that CAP detriment due to depressed vagal tone critically determines the severity of COVID-19. Keywords: COVID-19, Cytokine storm, Cholinergic anti-inflammatory pathway, NF-κB pathway, Vagal nerve, Stimulation, Heart rate variability
SARS-CoV-2 has set the world on fire The severe acute respiratory syndrome corona virus 2 (SARS-CoV-2) shows broad genetic similarities with other coronaviruses (SARS-CoV, SARS-CoV-RaTG13) (Palayew et al. 2020). However, its affinity to cellular angiotensin converting enzyme 2 (ACE 2) receptors is 10-fold higher than that of SARS-CoV (Wang et al. 2020a). This explains the high contagiousness, which led to a pandemic within a few months after its appearance in Wuhan in the People’s Republic of China. The explosive spread of COVID-19, caused by SARS-CoV-2, forced the World Health Organization (WHO) to declare a Public Health Emergency of International Concern (PHEIC) on January 30th (Wang et al. 2020a). Moreover, the consequences of this major threat to health care systems and the accompanying economic and social lockdown in most of the countries are incalculable. This underlines the urgent need for therapeutic and preventive solutions to combat COVID-19. In our clinical practice, the symptoms of SARS-CoV-2 infection presented along a wide range; from mild disease * Correspondence: [email protected] 1 Department of Anesthesiology, Helios Clinics, Colditzer Straße 48, 04703 Leisnig, Germany Full list of author information is available at the end of the article
courses with influenza-like symptoms up to acute respiratory distress syndrome (ARDS) (see Glossary), and death. Despite ARDS we saw patients with liver damage, severe intestinal dysfunction, rhabdomyolysis, acute renal failure, and coagulopathy with subsequent hemorrhage or embolism. In the critically-ill patients, we saw excessively high pro-inflammatory cytokine serum levels (interleukin 1β IL 1β (see Glossary), interleukin 6 – IL 6 (see Glossary), tumor necrosis factor α - TNF α (see Glossary), interleukin 8 – IL 8 (see Glossary)) and t
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