Discoveries

Why is it that two people can develop the same infection but have dramatically different disease trajectories? Salk scientist Janelle Ayres, PhD, and her colleagues discovered that the kidney plays a key role in filtering inflammatory molecules out of the body after an infection, and the amino acid methionine can improve that filtration. Dietary supplementation of methionine was enough to boost kidney performance in mice and protect against inflammation-related wasting, blood-brain barrier dysfunction, and death. The findings highlight how small dietary changes can lead to big impacts in disease outcomes and could support the use of methionine in future treatments for inflammatory conditions, especially in patients with kidney dysfunction. 

“Our findings add to a growing body of evidence that common dietary elements can be used as medicine. By studying these basic protective mechanisms, we reveal surprising new ways to shift individuals that are fated to develop disease and die onto trajectories of health and survival. It may one day be possible for something as simple as a supplement with dinner to make the difference between life and death for a patient.” 

JANELLE AYRES 

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How can two people infected by the same pathogen have such different responses? It largely comes down to variability in genetics (the genes you inherit) and life experience (your environmental, infection, and vaccination history). These two influences are imprinted on our cells through small molecular alterations called epigenetic changes, which shape cell identity and function by controlling which genes are turned “on” or “off.” Salk scientists, led by Joseph Ecker, PhD, debuted a new epigenetic catalog that reveals the distinct effects of genetic inheritance and life experience on various types of immune cells. The new cell-type-specific database helps explain why people can respond differently to the same illnesses and medications, and could serve as the foundation for more effective and personalized therapeutics.  

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Dealing with an infection isn’t as straightforward as simply killing the pathogen. Our bodies must carefully monitor and steer the immune response to tackle the infection without hurting healthy tissues. If the immune system overreacts and leads to sepsis, this can be more life-threatening than the original infection. 

But our bodies change a lot over the course of a lifetime. Do their mechanisms for regulating and tolerating immune activity change, too? Salk scientists, led by Janelle Ayres, PhD, found that younger and older mice with sepsis have distinct paths through sickness. In fact, the mechanisms that young mice used to survive sepsis were the very same mechanisms that caused older mice to die, suggesting that future therapies may be more effective if tailored to the patient’s age. The researchers say new sepsis treatments are especially needed as the antibiotic resistance crisis continues to threaten existing care strategies. 

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