ABSTRACT
In COVID-19, lung manifestations present as a slowly evolving pneumonia with insidious early onset interstitial pulmonary edema that undergoes acute exacerbation in the late stages and microvascular thrombosis. Currently, these manifestations are considered to be only consequences of pulmonary SARS-CoV-2 virus infection. We are proposing a new hypothesis that neurogenic insult may also play a major role in the pathogenesis of these manifestations. SARS-CoV-2 mediated inflammation of the nucleus tractus solitarius (NTS) may play a role in the acute exacerbation of pulmonary edema and microvascular clotting in COVID-19 patients.
Subject(s)
Coronavirus Infections/physiopathology , Hypotension/physiopathology , Lung/blood supply , Microvessels/physiopathology , Pneumonia, Viral/physiopathology , Pulmonary Edema/physiopathology , Solitary Nucleus/physiopathology , Thrombosis/physiopathology , Betacoronavirus , COVID-19 , Capillary Permeability/physiology , Coronavirus Infections/immunology , Cytokine Release Syndrome/immunology , Cytokine Release Syndrome/physiopathology , Facial Nerve , Glossopharyngeal Nerve , Humans , Inflammation , Lung/immunology , Microvessels/immunology , Pandemics , Parasympathetic Nervous System/physiopathology , Pneumonia, Viral/immunology , Pulmonary Edema/immunology , SARS-CoV-2 , Solitary Nucleus/immunology , Vagus Nerve , VasoconstrictionABSTRACT
Cytokine storm in COVID-19 is characterized by an excessive inflammatory response to SARS-CoV-2 that is caused by a dysregulated immune system of the host. We are proposing a new hypothesis that SARS-CoV-2 mediated inflammation of nucleus tractus solitarius (NTS) may be responsible for the cytokine storm in COVID 19. The inflamed NTS may result in a dysregulated cholinergic anti-inflammatory pathway and hypothalamic-pituitary-adrenal axis.