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. 2021 Jun 2;12:658896. doi: 10.3389/fimmu.2021.658896

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Copyright © 2021 Lange, Lange and Jaskuła

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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A cascade of events after SARS-CoV-2 infection starts with a few days time lag in which the virus replicates using a set of open frame genes in airway epithelial cells (70). Then pneumocytes are invaded and huge amount of DAMPS are released (71). After that innate immunity receptors recognize viral RNA and proinflammatory cytokines are produced using the NFkappaB signaling pathway. Pyroptosis is seen and proinflammatory cytokines build up an inflammatory response (72). Then macrophages, monocytes and polymorphonuclear leukocyte are recruited and activated in the inflammatory environment and the next wave of cytokines surges. In severe COVID-19 cases as a result of emergency myelopoiesis dysfunctional mature neutrophils and HLADRlow monocytes appear in the blood (73). In this complex situation the endothelial cell infection outcome contributes additionally to the inflammatory response. Endothelial damage leading to thrombolytic microangiopathy causes hypoxemia and malnutrition (43). The mTOR pathway is activated, which ends up with NFkappaB and massive cytokine release (74). Created in Biorender.com.