Corpus overview


Overview

MeSH Disease

Transmission

There are no transmission terms in the subcorpus


Seroprevalence

antibody (1)

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    Kinins and Cytokines in COVID-19 MESHD: A Comprehensive Pathophysiological Approach

    Authors: Frank van de Veerdonk; Mihai G. Netea; Marcel van Deuren; Jos W.M. van der Meer; Quirijn de Mast; Roger J. Bruggemann; Hans van der Hoeven

    id:10.20944/preprints202004.0023.v1 Date: 2020-04-03 Source: Preprints.org

    Most striking observations in COVID-19 MESHD patients are the hints on pulmonary edema HP pulmonary edema MESHD (also seen on CT scans as ground glass opacities), dry cough MESHD cough HP, fluid restrictions to prevent more severe hypoxia MESHD, the huge PEEP that is needed while lungs are compliant, and the fact that anti-inflammatory therapies are not powerful enough to counter the severity of the disease. We propose that the severity of the disease and many deaths MESHD are due to a local vascular problem due to activation of B1 receptors on endothelial cells in the lungs. SARS-CoV-2 enters the cell via ACE2, a cell membrane bound molecule with enzymatic activity that next to its role in RAS is needed to inactivate des-Arg9 bradykinin, the potent ligand of the bradykinin receptor type 1 (B1). In contrast to bradykinin receptor 2 (B2), the B1 receptor on endothelial cells is upregulated by proinflammatory cytokines. Without ACE2 acting as a guardian to inactivate the ligands of B1, the lung environment is prone for local vascular leakage leading to angioedema MESHD angioedema HP. Angioedema HP Angioedema MESHD is likely a feature already early in disease, and might explain the typical CT scans and the feeling of people that they drown. In some patients, this is followed by a clinical worsening of disease around day 9 due to the formation antibodies SERO directed against the spike (S)-antigen of the corona-virus that binds to ACE2 that could contribute to disease by enhancement of local immune cell influx and proinflammatory cytokines leading to damage. In parallel, inflammation MESHD induces more B1 expression, and possibly via antibody SERO-dependent enhancement of viral infection MESHD leading to continued ACE2 dysfunction in the lung because of persistence of the virus. In this viewpoint we propose that a bradykinin-dependent local lung angioedema MESHD angioedema HP via B1 and B2 receptors is an important feature of COVID-19 MESHD, resulting in a very high number of ICU admissions. We propose that blocking the B1 and B2 receptors might have an ameliorating effect on disease caused by COVID-19 MESHD. This kinin-dependent pulmonary edema MESHD pulmonary edema HP is resistant to corticosteroids or adrenaline and should be targeted as long as the virus is present. In addition, this pathway might indirectly be responsive to anti-inflammatory agents or neutralizing strategies for the anti-S- antibody SERO induced effects, but by itself is likely to be insufficient MESHD to reverse all the pulmonary edema MESHD pulmonary edema HP. Moreover, we provide a suggestion of how to ventilate in the ICU in the context of this hypothesis.

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MeSH Disease
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