1. Medicine
  2. Immunology and Inflammation
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Kallikrein-kinin blockade in patients with COVID-19 to prevent acute respiratory distress syndrome

  1. Frank L van de Veerdonk  Is a corresponding author
  2. Mihai G Netea
  3. Marcel van Deuren
  4. Jos WM van der Meer
  5. Quirijn de Mast
  6. Roger J Brüggemann
  7. Hans van der Hoeven
  1. Departments of Internal Medicine, Radboudumc Center for Infectious Diseases (RCI), Radboudumc, Netherlands
  2. Department for Genomics and Immunoregulation, Life and Medical Sciences Institute (LIMES), University of Bonn, Germany
  3. Department of Pharmacy, Radboudumc Center for Infectious Diseases (RCI), Radboudumc, Netherlands
  4. Intensive Care, Radboudumc Center for Infectious Diseases (RCI), Radboudumc, Netherlands
Short Report
Cite this article as: eLife 2020;9:e57555 doi: 10.7554/eLife.57555
3 figures

Figures

The kinin-kallikrein system and ACE/ACE2.

The pathways of processing of low-molecular-weight kininogen (LMWK) and high-molecular-weight kallikrein (HMWK) leading to Bradykinin 1 (B1) receptor agonists and Bradykinin 2 (B2) receptor agonists. CPM = carboxypeptidaseM; CPN = carboxypeptidaseN.

Schematic view of treatment strategies in COVID-19.
Alveolus in normal setting and during moderate and severe COVID-19, (A) normal, (B) mild inflammation, (C) hyperinflammation.

ACE2 downregulation by the SARS-CoV-2 is followed by loss of neutralizing capacity of Lys-des-arg9-bradykinin (BK) in the lung leading to plasma leakage. Subsequently plasma leakage results in more B1R ligands (des-arg9-BK) and B2R ligands (bradykinin).

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