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Initiation and resolution of inflammation are required to restore homeostasis. While neutrophils are classically viewed as short-lived effector cells that initiate inflammation, accumulating evidence suggests they can also contribute to resolution processes. Here, we identify neutrophil state characterized by long half-life, mitochondrial fitness, and reduced inflammatory output. Using myeloid- and neutrophil-restricted sphingosine 1-phosphate receptor-1 (S1PR1) overexpression mouse models (S1PR1), we show that elevated S1PR1 signaling is associated with redistribution of neutrophils from the bone marrow to peripheral tissues under steady-state conditions, without inducing overt inflammation or tissue injury. S1PR1 neutrophils exhibit reduced turnover , increased mitochondrial membrane potential and oxidative phosphorylation, and transcriptional programs linked to survival and dampened inflammatory signaling. Despite reduced oxidative burst, these neutrophils retain phagocytic capacity and antibacterial activity. In a model of influenza A virus infection, enhanced neutrophil-intrinsic S1PR1 signaling correlates with reduced lung injury, decreased inflammatory output, and improved survival. Together, these findings support a model in which S1PR1 tunes neutrophil persistence and inflammatory potential, thereby shaping immune responses during infection and tissue repair.