Found an aging "switch" that slows down wear and tear of the entire body

Scientists have found an immune "switch" whose deactivation slows down aging in multiple organs at once. It turns out that with age, immune cells stop clearing "aged" neutrophils in time, and this fuels chronic inflammation throughout the entire body. The study was published in the journal Science.

Neutrophils are the most abundant immune cells in the blood; every day the body needs to dispose of about 100 billion of them. Just 8–12 hours after entering the bloodstream, they "age" and begin to malfunction, and if they are not cleared in time, they damage tissues and sustain inflammation, which scientists consider one of the driving forces of aging.

Researchers led by Jesse Tan and Katrin Andreasson from Stanford School of Medicine discovered that tissue macrophages are responsible for clearing these cells, and that a receptor called EP2 hinders their work. When the scientists blocked this receptor in mice, macrophages once again began effectively clearing the body of aged neutrophils.

The effect turned out to be extensive. During normal aging in mice, the levels of 71 blood proteins changed significantly, but in animals lacking the EP2 receptor, a full 59 of them remained at "youthful" levels. In other words, disabling a single receptor kept organs younger and reduced inflammation throughout the entire body.

The experiments were conducted on mice aged 23–25 months, which roughly corresponds to a human aged 60–70 years. "Aged neutrophils are killing our tissues. Their timely removal is necessary to prevent chronic inflammation," the authors noted. They hope that targeting this mechanism will in the future help slow age-related diseases in humans, although for now the research involves animal experiments. The scientists are additionally encouraged by the fact that the target is a single receptor — meaning that, in theory, a precisely targeted drug could be developed for it.