tetano
Editor, Senior Moderator
J Infect Dis
. 2020 Oct 10;jiaa646.
doi: 10.1093/infdis/jiaa646. Online ahead of print.
Complement activation in the disease course of COVID-19 and its effects on clinical outcomes
Aline H de Nooijer[SUP] 1 [/SUP], Inge Grondman[SUP] 1 [/SUP], Nico A F Janssen[SUP] 1 [/SUP], Mihai G Netea[SUP] 1 2 [/SUP], Loek Willems[SUP] 3 [/SUP], Frank L van de Veerdonk[SUP] 1 [/SUP], Evangelos J Giamarellos-Bourboulis[SUP] 4 [/SUP], Erik J M Toonen[SUP] 3 [/SUP], Leo A B Joosten[SUP] 1 5 [/SUP]
Affiliations
Abstract
Background: Excessive activation of immune responses in coronavirus disease 2019 (COVID-19) is considered to be related to disease severity, complications and mortality. The complement system is an important component of innate immunity and can stimulate inflammation, but its role in COVID-19 is unknown.
Methods: A prospective, longitudinal, single center study was performed in hospitalized COVID-19 patients. Plasma concentrations of complement factors C3a, C3c, and terminal complement complex (TCC) were assessed at baseline and during hospital admission. In parallel, routine laboratory and clinical parameters were collected from medical files and analyzed.
Results: Complement factors C3a, C3c and TCC were significantly increased in plasma of COVID-19 patients compared to healthy controls (p<0.05). These complement factors were especially elevated in ICU patients during the entire disease course (p<0.005 for C3a and TCC). More intense complement activation was observed in patients that deceased and in patients with thromboembolic events.
Conclusions: COVID-19 patients demonstrate activation of the complement system, which is related to disease severity. This pathway may be involved in the dysregulated pro-inflammatory response associated with increased mortality and thromboembolic complications. Components of the complement system might have potential as prognostic markers for disease severity and as therapeutic targets in COVID-19.
Keywords: ARDS; COVID-19; Coagulation; Complement; Inflammation; SARS-CoV-2.
. 2020 Oct 10;jiaa646.
doi: 10.1093/infdis/jiaa646. Online ahead of print.
Complement activation in the disease course of COVID-19 and its effects on clinical outcomes
Aline H de Nooijer[SUP] 1 [/SUP], Inge Grondman[SUP] 1 [/SUP], Nico A F Janssen[SUP] 1 [/SUP], Mihai G Netea[SUP] 1 2 [/SUP], Loek Willems[SUP] 3 [/SUP], Frank L van de Veerdonk[SUP] 1 [/SUP], Evangelos J Giamarellos-Bourboulis[SUP] 4 [/SUP], Erik J M Toonen[SUP] 3 [/SUP], Leo A B Joosten[SUP] 1 5 [/SUP]
Affiliations
- PMID: 33038254
- DOI: 10.1093/infdis/jiaa646
Abstract
Background: Excessive activation of immune responses in coronavirus disease 2019 (COVID-19) is considered to be related to disease severity, complications and mortality. The complement system is an important component of innate immunity and can stimulate inflammation, but its role in COVID-19 is unknown.
Methods: A prospective, longitudinal, single center study was performed in hospitalized COVID-19 patients. Plasma concentrations of complement factors C3a, C3c, and terminal complement complex (TCC) were assessed at baseline and during hospital admission. In parallel, routine laboratory and clinical parameters were collected from medical files and analyzed.
Results: Complement factors C3a, C3c and TCC were significantly increased in plasma of COVID-19 patients compared to healthy controls (p<0.05). These complement factors were especially elevated in ICU patients during the entire disease course (p<0.005 for C3a and TCC). More intense complement activation was observed in patients that deceased and in patients with thromboembolic events.
Conclusions: COVID-19 patients demonstrate activation of the complement system, which is related to disease severity. This pathway may be involved in the dysregulated pro-inflammatory response associated with increased mortality and thromboembolic complications. Components of the complement system might have potential as prognostic markers for disease severity and as therapeutic targets in COVID-19.
Keywords: ARDS; COVID-19; Coagulation; Complement; Inflammation; SARS-CoV-2.