Extracellular adenosine is a biologically active signaling molecule that accumulates at sites of metabolic stress in sepsis. Extracellular adenosine has potent immunosuppressive effects by binding to and activating G protein-coupled A adenosine receptors (AARs) on the surface of neutrophils. AAR signaling reproduces many of the phenotypic changes in neutrophils that are characteristic of sepsis, including decreased degranulation, impaired chemotaxis, and diminished ability to ingest and kill bacteria. We hypothesized that AARs also suppress neutrophil aging, which precedes cell death, and N1 to N2 polarization. Using human neutrophils isolated from healthy subjects, we demonstrate that AAR stimulation slows neutrophil aging, suppresses cell death, and promotes the polarization of neutrophils from an N1 to N2 phenotype. Using genetic knockout and pharmacological blockade, we confirmed that AARs decrease neutrophil aging in murine sepsis induced by cecal ligation and puncture. AARs expression is increased in neutrophils from septic patients compared to healthy subject but AAR expression fails to correlate with aging or N1/N2 polarization. Our data reveals that AARs regulate neutrophil aging in healthy but not septic neutrophils.