Chronic Lung Diseases (CLDs) are prevalent in aging and marked by reduced repair and regenerative capacity ofalveolar progenitor cells. Aging induces low, chronic inflammation (inflammaging), which, combined with environmental factors, increases CLD susceptibility. While research has focused on susceptibility mechanisms, less is understood about early-life control of lung regenerative capacity. To address this, we isolated epithelial cells from mice across the lifespan, including neonates, young adults, and old mice. RNA sequencing revealed age-dependent enrichment of pathways related to senescence, inflammation, stemness, and injury in epithelial cells. To examine regenerative capacity across ages, we developed a murine neonatal alveolar organoid model. Neonatal organoids exhibited significantly higher regenerative capacity (187%±70%) and markers for immune and stem cell activity, including elevated WNT signaling, compared to adult organoids, as analyzed by multiplex FACS and IF. Organoids from aged mice retained a pro-inflammatory profile, suggesting cell-intrinsic sources of inflammaging. We exposed organoids to disease-relevant stimuli to assess CLD susceptibility. Neonatal organoids showed greater resilience and an increase in activated progenitor cells, which was reduced when exposed to inflammatory mediators from the inflammaged niche. Additionally, activation of neonatal-enriched pathways, such as WNT, enhanced regenerative capacity in aged cells. In summary, lung regeneration and resilience over the life span is promoted by cell-intrinsic mechanisms that are propagated by alveolar epithelial cells and associated with immune homeostasis that can be exploited to tune regenerative capacity.