tetano
Editor, Senior Moderator
Front Immunol
. 2020 Jul 21;11:1714.
doi: 10.3389/fimmu.2020.01714. eCollection 2020.
COVID-19: Underlying Adipokine Storm and Angiotensin 1-7 Umbrella
Geoffroy M?ry[SUP] 1 [/SUP], Olivier Epaulard[SUP] 2 3 4 [/SUP], Anne-Laure Borel[SUP] 5 6 [/SUP], Bertrand Toussaint[SUP] 7 8 [/SUP], Audrey Le Gouellec[SUP] 7 8 [/SUP]
Affiliations
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the third coronavirus leading to a global health outbreak. Despite the high mortality rates from SARS-CoV-1 and Middle-East respiratory syndrome (MERS)-CoV infections, which both sparked the interest of the scientific community, the underlying physiopathology of the SARS-CoV-2 infection, remains partially unclear. SARS-CoV-2 shares similar features with SARS-CoV-1, notably the use of the angiotensin conversion enzyme 2 (ACE2) as a receptor to enter the host cells. However, some features of the SARS-CoV-2 pandemic are unique. In this work, we focus on the association between obesity, metabolic syndrome, and type 2 diabetes on the one hand, and the severity of COVID-19 infection on the other, as it seems greater in these patients. We discuss how adipocyte dysfunction leads to a specific immune environment that predisposes obese patients to respiratory failure during COVID-19. We also hypothesize that an ACE2-cleaved protein, angiotensin 1-7, has a beneficial action on immune deregulation and that its low expression during the SARS-CoV-2 infection could explain the severity of infection. This introduces angiotensin 1-7 as a potential candidate of interest in therapeutic research on CoV infections.
Keywords: ACE2; SARS-CoV; adipocyte; coronavirus; inflammation; metabolic syndrome; obesity.
. 2020 Jul 21;11:1714.
doi: 10.3389/fimmu.2020.01714. eCollection 2020.
COVID-19: Underlying Adipokine Storm and Angiotensin 1-7 Umbrella
Geoffroy M?ry[SUP] 1 [/SUP], Olivier Epaulard[SUP] 2 3 4 [/SUP], Anne-Laure Borel[SUP] 5 6 [/SUP], Bertrand Toussaint[SUP] 7 8 [/SUP], Audrey Le Gouellec[SUP] 7 8 [/SUP]
Affiliations
- PMID: 32793244
- PMCID: PMC7385229
- DOI: 10.3389/fimmu.2020.01714
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the third coronavirus leading to a global health outbreak. Despite the high mortality rates from SARS-CoV-1 and Middle-East respiratory syndrome (MERS)-CoV infections, which both sparked the interest of the scientific community, the underlying physiopathology of the SARS-CoV-2 infection, remains partially unclear. SARS-CoV-2 shares similar features with SARS-CoV-1, notably the use of the angiotensin conversion enzyme 2 (ACE2) as a receptor to enter the host cells. However, some features of the SARS-CoV-2 pandemic are unique. In this work, we focus on the association between obesity, metabolic syndrome, and type 2 diabetes on the one hand, and the severity of COVID-19 infection on the other, as it seems greater in these patients. We discuss how adipocyte dysfunction leads to a specific immune environment that predisposes obese patients to respiratory failure during COVID-19. We also hypothesize that an ACE2-cleaved protein, angiotensin 1-7, has a beneficial action on immune deregulation and that its low expression during the SARS-CoV-2 infection could explain the severity of infection. This introduces angiotensin 1-7 as a potential candidate of interest in therapeutic research on CoV infections.
Keywords: ACE2; SARS-CoV; adipocyte; coronavirus; inflammation; metabolic syndrome; obesity.