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

Scientists have found an immune "switch" whose deactivation slows down aging in multiple organs simultaneously. It turned 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 has to dispose of approximately 100 billion of them. Just 8–12 hours after entering the bloodstream, they "age" and begin to malfunction. If they are not cleared in time, they damage tissues and sustain low-grade inflammation, which scientists consider one of the main driving forces of aging.

A research team led by Jesse Tan and Katrin Andreasson from Stanford School of Medicine discovered that tissue macrophages are responsible for clearing these cells, and a receptor called EP2 prevents them from coping with this task. When the scientists blocked this receptor in mice, macrophages once again began effectively clearing the body of aged neutrophils.

The result was impressive. During normal aging, levels of 71 blood proteins changed significantly in mice, while in animals with the EP2 receptor deactivated, a full 59 of them remained at "youthful" levels. In effect, switching off 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 60–70 years of human life. "Aged neutrophils are killing our tissues. Their timely removal is necessary to prevent chronic inflammation," the authors emphasized. 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.