Apart from weakened immunity, there is another factor that determines whether COVID can cause serious infection and that is the dysfunctional endothelium, in more simple words, the vascular system, cited a recent study. Several clinical signs, such as destruction of blood vessels in the lungs and acute respiratory distress syndrome, point to effects on the endothelium, it also said.
‘In our study, we investigated which immune cells are activated in severe cases and how the endothelium, in other words, blood vessels, and their activation plays a role in disease progression,’ explained Professor Christine Falk, Scientist Hannover Medical School (MHH) and the German Center for Infection Research (DZIF). The study is published in the Journal of Signal Transduction and Targeted Therapy.
What is Endothelium and how can COVID affect it?
Endothelium is a thin layer of cells that line blood vessels, forming a barrier between blood flow and surrounding tissue.
COVID infection can cause strong activation of the immune system and endothelial cells in the lungs, resulting in the release of various soluble plasma proteins. Severe COVID-19 cases are associated with dysfunction of the endothelium, in which the barrier between the alveoli (the small air sacs inside your lungs) and the surrounding vessels is no longer intact.
How serious is the damage?
During the study, the researchers observed that there are seven plasma proteins that are associated with the severe form of the disease. They can cause severe inflammation that can permanently damage the endothelial barrier.
Furthermore, recovery from severe COVID-19 cases appears to be related to the regeneration of this endothelial barrier.
Currently, investigations are underway to determine whether endothelial inflammation with an overreaction of T-lymphocytes (which play a central role in the adaptive immune response) can lead to permanent damage, the extent to which lung regenerates. is affected and the nervous system is affected. ,
Which immune cells were detected in COVID-19 ICU patients?
The study showed excessive activation of T-lymphocytes and natural killer cells, as well as the development of memory T-cells and strong proliferation of plasmablasts, cells that can produce large amounts of antibodies.
In addition, COVID patients in ICU had higher levels of spike- and nucleocapsid-specific antibodies. And the immune cell phenotype of these patients mainly changed over time and was less related to the progressive severity of the disease.
The progression of COVID-19, on the other hand, was closely linked to increased levels of various soluble plasma proteins, namely some inflammatory mediators, and endothelial factors in particular.
“We were able to demonstrate that ICU patients with COVID-19 can be divided into different groups based on their plasma protein profile, which is associated with disease severity”, lead author, PhD, doctoral student at MHH Louisa Ruhl explained.
How do activated immune cells act on endothelial cells?
Christine Falk’s team now wants to investigate which elements of the immune system cause activation and damage of the endothelium and whether strong activation of the immune system leads to the development of virus-specific T-lymphocytes that recognize and destroy infected cells. can and thus contribute to over-reaction.
The study showed that there were also changes in the immune cell repertoire in recovered ICU patients with COVID-19. This may be related to the development of long-term COVID cases.
(with inputs from agencies)
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