Restored clearance of senescent neutrophils by tissue-resident macrophages limits organ aging

Y Yuting Jessy Tan (Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.) T Travis E. Conley (Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.) F Fuwen Yao (Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.) F Fernando J. García-Marqués (Department of Radiology, Stanford University School of Medicine, Palo Alto, CA, USA.) D Damilola E. Akinyemi (Institute for Experimental Pathology (ExPat), Centre for Molecular Biology of Inflammation (ZMBE), University of Münster, Münster, NRW, Germany.) V Van Vuong Dinh (Institute for Experimental Pathology (ExPat), Centre for Molecular Biology of Inflammation (ZMBE), University of Münster, Münster, NRW, Germany.) Q Qian Wang A Abel Bermudez (Department of Radiology, Stanford University School of Medicine, Palo Alto, CA, USA.) J Jieun Kim (Neurosciences Preclinical Imaging Laboratory, Wu Tsai Neurosciences Institute, Stanford University, Stanford, CA, USA.) J Julia A. Belk O Oliver Soehnlein S Sharon J. Pitteri (Department of Radiology, Stanford University School of Medicine, Palo Alto, CA, USA.) K Katrin I. Andreasson (Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.)

Abstract

Aging disrupts tissue homeostasis across organ systems. Here, we identify tissue-resident macrophages (TRMs) as central coordinators of age-related organ decline through impaired clearance of senescent neutrophils, a process regulated by the immunomodulatory prostaglandin E2 (PGE 2 ) receptor EP2. Reducing TRM EP2 signaling in aged mice preserved youthful mitochondrial fitness and prevented cognitive decline, frailty, sarcopenia, adiposity, cardiac impairment, and systemic inflammation. Plasma proteomics implicated the liver as a major source of age-associated immune change, in which reduced TRM EP2 signaling rescued neutrophil efferocytosis and prevented paracrine stress in neighboring cells. Elevated TRM EP2 expression and senescent neutrophils were also observed in aged and diseased human tissues. Pharmacologic EP2 inhibition restored youthful neutrophil clearance, establishing impaired TRM efferocytosis as a reversible driver of organ decline in aging.

Article Details

Journal Science
Volume / Issue Vol. 393, Issue 6808
Published July 16, 2026
ISSN 0036-8075
Publisher American Association for the Advancement of Science

Journal Info

Science

American Association for the Advancement of Science

ISSN: 0036-8075 Social Sciences

Authors (13)

Y

Yuting Jessy Tan

Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.

T

Travis E. Conley

Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.

F

Fuwen Yao

Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.

F

Fernando J. García-Marqués

Department of Radiology, Stanford University School of Medicine, Palo Alto, CA, USA.

D

Damilola E. Akinyemi

Institute for Experimental Pathology (ExPat), Centre for Molecular Biology of Inflammation (ZMBE), University of Münster, Münster, NRW, Germany.

V

Van Vuong Dinh

Institute for Experimental Pathology (ExPat), Centre for Molecular Biology of Inflammation (ZMBE), University of Münster, Münster, NRW, Germany.

Q

Qian Wang

A

Abel Bermudez

Department of Radiology, Stanford University School of Medicine, Palo Alto, CA, USA.

J

Jieun Kim

Neurosciences Preclinical Imaging Laboratory, Wu Tsai Neurosciences Institute, Stanford University, Stanford, CA, USA.

J

Julia A. Belk

O

Oliver Soehnlein

S

Sharon J. Pitteri

Department of Radiology, Stanford University School of Medicine, Palo Alto, CA, USA.

K

Katrin I. Andreasson

Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.