Innate immune system aggravates severe COVID-19


In critically ill COVID-19 patients, the innate immune system is strongly activated which can cause thrombosis and reduced oxygenation in the patients. This is shown in a study from IGP, published in the journal Frontiers in Immunology.

The blood contains a large number of proteins that make up the body’s first barrier to both recognise and destroy microorganisms, including SARS-CoV-2, the virus causing COVID-19. These proteins are part of the intravascular innate immune system (IIIS) which consists of some of the white blood cell types, blood platelets and the cascade systems.

Only 5 per cent of present-day mammals have an immune system with T cells and B cells, while the rest only rely on the natural immune system, which to large extent consists of IIIS. IIIS has a native capacity to recognise and eliminate foreign substances and particles such as microorganisms and damaged cells. This allows the IIIS to function as a “waste cleaning system”.

In the present study, the researchers have during 2020 studied 66 critically ill COVID‑19 patients that were treated at an intensive care unit and found a strong activation of IIIS.

“It was probably the tissue damage, with dead cells in the lungs, that initiated this activation. It can potentially lead to thrombosis and reduced oxygenation due to increased leakage in the blood vessels," says Bo Nilsson at IGP who has led the study.

Since the level of activation is prognostically linked to survival and lung function, the new findings also support the hypothesis that IIIS is one of the drivers for severe COVID-19. An explanation for this behaviour of IIIS in some COVID-19 patients could be that the cell damage is so grave that the IIIS over-reacts and destroys the tissue instead of helping cleaning it

If the IIIS has the role that the researchers suspect, this suggests that already approved drugs that are used to treat the disease hereditary angioedema could be used to treat severe COVID-19.

The study has been performed in collaboration with researchers at the Department of Surgical Sciences and Department of Medical Cell Biology, Uppsala University, Lund University and the University Hospital in Ulm, Germany.

More information:
Paper in Frontiers in Immunology
Bo Nilsson’s research