Moreover, IL-6 signaling induces the secretion by ECs of more IL-6 and other cytokines. Binding of IL-6 and IL-2 on their receptors induces a capillary leak. Soluble IL-2R (sIL-2R) is mostly secreted by activated T helper lymphocytes, but might be also secreted by ECs. ECs express both IL-6 receptor (IL-6R) and IL-2R on their surface. b In patients diagnosed with severe COVID-19, increased levels of pro-inflammatory cytokines, in particular, the soluble interleukin 2-receptor (IL-2R) and interleukin-6 (IL-6) have been observed. Moreover, a protease TMPRSS2 inhibitor is efficient to block SARS-CoV-2 entry into the endothelial cells (ECs). The recombinant protein of human ACE2 fused with the Fc region of the human immunoglobulin IgG1 (rACE2-IgG1) binds with high affinity to the receptor-binding domain of SARS-CoV-2. Cell invasion also depends on the presence of the protease Transmembrane protease serine 2 (TMPRSS-2) that is able to cleave the viral spike. a Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) binds with Angiotensin- converting enzyme 2 (ACE2) on the cell membrane of the host cells. The role of endothelial cells in SARS-CoV-2 infection and treatment. Studies focusing on endothelial dysfunction in COVID-19 patients are warranted as to decipher their precise role in severe SARS-CoV-2 infection and organ dysfunction and to identify targets for further interventions.ĬOVID-19 Cytokines Endothelial cells Endothelial dysfunction SARS-CoV-2 Thrombosis. Ongoing trials directly and indirectly target COVID-19-related endothelial dysfunctions: i.e., a virus-cell entry using recombinant angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS-2) blockade, coagulation activation, and immunomodulatory therapies, such as anti-IL-6 strategies. ![]() COVID-19-induced endotheliitis may explain the systemic impaired microcirculatory function in different organs in COVID-19 patients. The pro-inflammatory cytokine storm, with elevated levels of interleukin-6 (IL-6), IL-2 receptor, and tumor necrosis factor-α, could also participate in endothelial dysfunction and leukocyte recruitment in the microvasculature. ![]() Venous thrombotic events, particularly pulmonary embolism, with elevated D-dimer and coagulation activation are highly prevalent in COVID-19 patients. In severe SARS-CoV-2 infections, emerging data including recent histopathological studies have emphasized the crucial role of endothelial cells (ECs) in vascular dysfunction, immunothrombosis, and inflammation.Histopathological studies have evidenced direct viral infection of ECs, endotheliitis with diffuse endothelial inflammation, and micro- and macrovascular thrombosis both in the venous and arterial circulations.
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