SARS-CoV-2 as a Factor to Disbalance the Renin-Angiotensin System: A Suspect in the Case of Exacerbated IL-6 Production

Fever in infections correlates with inflammation, macrophage infiltration into the affected organ, macrophage activation, and release of cytokines involved in immune response, hematopoiesis, and homeostatic processes. Angiotensin-converting enzyme 2 (ACE2) is the canonical cell surface receptor for...

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Veröffentlicht in:The Journal of immunology (1950) 2020-09, Vol.205 (5), p.1198-1206
Hauptverfasser: Franco, Rafael, Rivas-Santisteban, Rafael, Serrano-Marín, Joan, Rodríguez-Pérez, Ana I, Labandeira-García, José L, Navarro, Gemma
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Sprache:eng
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Zusammenfassung:Fever in infections correlates with inflammation, macrophage infiltration into the affected organ, macrophage activation, and release of cytokines involved in immune response, hematopoiesis, and homeostatic processes. Angiotensin-converting enzyme 2 (ACE2) is the canonical cell surface receptor for SARS-CoV-2. ACE2 together with angiotensin receptor types 1 and 2 and ACE2 are components of the renin-angiotensin system (RAS). Exacerbated production of cytokines, mainly IL-6, points to macrophages as key to understand differential COVID-19 severity. SARS-CoV-2 may modulate macrophage-mediated inflammation events by altering the balance between angiotensin II, which activates angiotensin receptor types 1 and 2, and angiotensin 1-7 and alamandine, which activate proto-oncogene and -related D receptors, respectively. In addition to macrophages, lung cells express RAS components; also, some lung cells are able to produce IL-6. Addressing how SARS-CoV-2 unbalances RAS functionality via ACE2 will help design therapies to attenuate a COVID-19-related cytokine storm.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.2000642