Organ ‘Crosstalk’ Extends Harms of Inflammation from Liver to Brain

As people age, the liver is among several organs that experience chronic, low-grade inflammation, a state that keeps the immune system activated even though there is no threat.

Liver inflammation has been linked to several liver diseases, such as fatty liver disease and liver cancer, but the liver also communicates with the brain, triggering inflammation that can lead to cognitive decline. University of Oklahoma researcher Deepa Sathyaseelan, Ph.D., recently earned a $2 million grant from the National Institutes of Health to study the reasons behind this liver-brain crosstalk and test methods of protecting both organs.

Specifically, Sathyaseelan is studying necroptosis, which is a natural form of cell death with a downside: Cells that die through necroptosis burst and release substances that lead to inflammation. In previously published research involving an aging mouse model, Sathyaseelan and her team demonstrated the damaging effects of necroptosis in the liver, as well as the reduction of those effects when necroptosis was blocked. They also found that activating necroptosis in the liver increased liver inflammation and, surprisingly, increased brain inflammation, which affected the mice’s ability to build nests, a possible sign of cognitive impairment.

On the strength of those studies, she earned this new NIH grant to better understand how necroptosis of liver cells causes the inflammation that affects both the liver and the brain with age. Such knowledge is crucial for ultimately devising a way to reduce inflammation and improve tissue function.

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