Overview
- Researchers found older mice accumulate senescent neutrophils in organs because tissue‑resident macrophages lose the ability to clear them.
- The loss of clearance was traced to elevated prostaglandin E2 activity overstimulating the EP2 receptor on those macrophages.
- Genetic targeting of EP2 in macrophages and an experimental oral EP2 blocker each increased removal of senescent neutrophils and improved inflammation, muscle mass, mobility and memory in aged mice.
- Analysis of human liver samples showed higher EP2 activity and more senescent neutrophils but the human data are correlative and do not show that EP2 blockade restores clearance in people.
- Experts warn EP2 has normal roles across the body so systemic blockade could cause harm, and researchers plan follow‑up studies to test disease links and safer, targeted ways to translate the finding.