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Cytokine storm barrier

Researchers from the U.S. and Brazil have found that the protein slit homolog 2 can prevent tissue damage and death caused by the cytokine storm during bacterial sepsis or severe viral infections.1 Navigen Pharmaceuticals has in-licensed the findings and thinks the protein's enhancement of vascular stability could be more effective at treating hypercytokinemia than strategies that target individual cytokines.

As part of the body's normal inflammatory response to bacterial and viral infections, immune cells secrete proinflammatory cytokines that disrupt intercellular interactions between cellular adhesion molecules that form the vascular barrier. This allows immune cells to permeate the barrier and reach infected tissues.

After moving across the vascular barrier, the immune cells ordinarily close the cytokine-induced gaps. But during sepsis and other severe infections, the inflammatory response can spiral out of control, resulting

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