COVID-19 vaccinated individuals may be ill…See more

When a second type of immune cell — T cells, which serve as roving sentinels capable of recognizing specific threats and amplifying immune responses — was introduced to the dish, or even when T cells were simply placed in the fluid in which vaccine-treated macrophages had been bathed, IFN-gamma output increased dramatically. T cells exposed to the vaccine alone, without the macrophage-conditioned environment, produced only ordinary amounts of IFN-gamma. This finding established a clear sequence: macrophages are the primary source of CXCL10, and T cells are the primary source of IFN-gamma, with the latter depending on signals from the former.

Confirming the Damage in Living Systems

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To confirm that this two-protein cascade actually causes cardiac injury, the researchers turned to mouse models. Young male mice were vaccinated and subsequently showed elevated levels of cardiac troponin — a protein released into the bloodstream when heart muscle cells are damaged and a standard clinical marker used to diagnose heart injury in humans.

Examination of the mice’s heart tissue revealed infiltration by macrophages and neutrophils, another class of aggressive immune cells. This kind of immune cell invasion into heart tissue is also observed in human patients with post-vaccination myocarditis. The problem with these cells is that, in their eagerness to fight perceived threats, they can cause collateral damage to healthy tissue — including the delicate cells of the heart muscle.

When the researchers blocked the activity of CXCL10 and IFN-gamma, this infiltration was substantially reduced, and cardiac troponin levels dropped, even as the overall immune response to the vaccine remained largely intact. This was a critical finding: it suggested that the inflammatory damage to the heart might be separable from the vaccine’s protective immune function.

The team went further, using a cutting-edge technology developed in Wu’s laboratory. Human skin or blood cells can be transformed into blank stem-like cells and then guided to differentiate into heart muscle cells, macrophages, and the cells that line blood vessels. These cells can then be assembled into tiny spherical structures that mimic the beating, contracting behavior of actual heart tissue — what the researchers call “cardiac spheroids.”

When these cardiac spheroids were treated with cytokine-enriched fluid from vaccine-stimulated immune cells, markers of cardiac stress increased significantly and the spheroids’ ability to contract rhythmically was impaired. When cytokine inhibitors were applied, much of this damage was reversed.

A Soybean Compound Enters the Picture

Having mapped out the mechanism of injury, Wu and his team turned to a question with practical implications: could anything be done to prevent it?Continue reading…