The ongoing
COVID-19 pandemic has caused significant morbidity and mortality worldwide, as well as profound effects on society.
COVID-19 patients have an increased risk of thromboembolic (TE) complications, which develop despite pharmacological thromboprophylaxis. The mechanism behind COVID-19-associated coagulopathy remains unclear.
Mannose-binding lectin (MBL), a pattern recognition molecule that initiates the
lectin pathway of complement activation, has been suggested as a potential amplifier of blood coagulation during
thromboinflammation. Here we describe data from a cohort of
critically ill COVID-19 patients (n = 65) treated at a tertiary hospital center intensive care unit (ICU). A subset of patients had strongly elevated MBL plasma levels, and activity upon ICU admission, and patients who developed symptomatic TE (14%) had significantly higher MBL levels than patients without TE. MBL was strongly correlated to plasma
D-dimer levels, a marker of
COVID-19 coagulopathy, but showed no relationship to degree of
inflammation or other organ dysfunction. In conclusion, we have identified complement activation through the MBL pathway as a novel amplification mechanism that contributes to pathological
thrombosis in
critically ill COVID-19 patients. Pharmacological targeting of the MBL pathway could be a novel treatment option for
thrombosis in
COVID-19. Laboratory testing of MBL levels could be of value for identifying
COVID-19 patients at risk for TE events.