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Alveolar macrophages (AMs) are resident immune cells of the lung that are critical for host defense. AMs are capable of proliferative renewal, yet their numbers are known to decrease with aging and increase with cigarette smoking. The mechanism by which AM proliferation is physiologically restrained, and whether dysregulation of this brake contributes to altered AM numbers in pathologic circumstances, however, remains unknown. Mice of advanced age exhibited diminished basal AM numbers and contained elevated PGE 2 levels in their bronchoalveolar lavage fluid (BALF) as compared with young mice. Exogenous PGE 2 inhibited AM proliferation in an E prostanoid receptor 2 (EP2)-cyclic AMP-dependent manner. Furthermore, EP2 knockout (EP2 KO) mice exhibited elevated basal AM numbers, and their AMs resisted the ability of PGE 2 and aged BALF to inhibit proliferation. In contrast, increased numbers of AMs in mice exposed to cigarette smoking were associated with reduced PGE 2 levels in BALF and were further exaggerated in EP2 KO mice. Collectively, our findings demonstrate that PGE 2 functions as a tunable brake on AM numbers under physiologic and pathophysiological conditions.

PGE2accounts for bidirectional changes in alveolar macrophage self-renewal with aging and smoking

PGE₂accounts for bidirectional changes in alveolar macrophage self-renewal with aging and smoking