Endovascular profiles linked to neutrophil activation in children and young adults with long COVID, 2026, Steifman, VanElzakker, Yonker+

SNT Gatchaman

SNT Gatchaman

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Endovascular profiles linked to neutrophil activation in children and young adults with long COVID
Steifman, Carly B; Alvarez-Carcamo, Bryan; Verma, Smriti; McCarthy, Ronan; Guthrie, Lauren B; Gill, Kirandeep K; Swank, Zoe; Walt, David R; Grabowski, Eric F; Fasano, Alessio; VanElzakker, Michael B; Irimia, Daniel; Yonker, Lael M

Endovascular symptoms are among the most debilitating long COVID symptoms; however, underlying mechanisms are unclear. Children and young adults with long COVID, an understudied population, offer key insight into long COVID pathology.

Eighty-four children and young adults ≤25 years from the U.S. and Canada were enrolled; 61 with long COVID and 23 healthy pediatric controls. We assessed symptom burden, quantified fibrin amyloid microclots, endovascular cytokines, cell-free DNA, and conducted in vitro assays to assess Spike-related neutrophil-mediated endothelial cell injury.

Cardiovascular symptoms were prevalent among participants with long COVID. Microclot burden was increased (p = 0.0003), as were markers of angiogenesis and endothelial remodeling, including FGF-2, which correlated with microclots (p = 0.04). Cytokines involved in leukocyte trafficking (sVCAM-1, L-selectin, α-2-macroglobulin) were reduced while cell-free DNA, a marker of intravascular neutrophil extracellular trap (NET) formation, was increased (p = 0.003) and positively correlated with microclot component serum amyloid A (p = 0.004). Co-culture assays revealed that NETosis, triggered by Spike immune complexes, contributes to endothelial injury in long COVID.

Children and young adults with long COVID with cardiovascular symptoms display increased microclots, endothelial injury, and neutrophil inflammation, which warrant further evaluation and suggest intravascular NETosis as a key driver of endovascular pathology in long COVID.

Web | DOI | PDF | Nature Pediatric Research | Open Access
 
It comes across as complete make-believe. The authors do not appear to have any idea what the words mean.

Sadly, that comes as no surprise. I hear seminars in my own department made up of this sort of Chinese whisper salad.
 
Removing spike proteins, often associated with Long COVID or post-vaccination syndromes, involves supporting the body’s detoxification and immune systems to degrade and eliminate these proteins. Common strategies include using proteolytic enzymes like nattokinase and bromelain, promoting autophagy through fasting, and using compounds like zinc and curcumin.

There are other ways to promote autophagy for those of us who don't do well with fasting.

Strategies for the Management of Spike Protein-Related Pathology​


Strategies for the Management of Spike Protein-Related Pathology - PMC

In the wake of the COVID-19 crisis, a need has arisen to prevent and treat two related conditions, COVID-19 vaccine injury and long COVID-19, both of which can trace at least part of their aetiology to the spike protein, which can cause harm through ...
pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov
 
med.stanford.edu

Stanford Medicine study shows why mRNA COVID-19 vaccine can cause myocarditis

COVID-19 — and, less frequently, the mRNA-based COVID-19 vaccine — can cause inflamed heart tissue in some people. A new study implicates a pair of substances secreted by immune cells and proposes a strategy to mitigate the vaccine effect.
med.stanford.edu med.stanford.edu


These results showed that macrophages are the chief source of CXCL10 and that T cells are the chief source of IFN-gamma in response to mRNA vaccination.

This macrophage and neutrophil infiltration into the heart — which comes at a cost, as these shoot-first-and-ask-questions-later warrior immune cells often unload friendly fire, causing collateral damage to healthy tissue, including heart muscle — could be minimized by blocking CXCL10 and IFN-gamma activity.

Also seen in the mice’s hearts were increased populations of cell-surface molecules that snag macrophages, neutrophils and other white-blood-cell types, causing them to adhere to endothelial cells, which line all blood vessels including those in the heart.

If any of the links that I post are counterproductive to the preprint, let me know and I will delete them.
 
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