Nanoplastics target lung monocytes, disrupting immune dynamics

interstitial macrophages selectively sequestered nanoplastics, whereas in the blood, sequestration was restricted exclusively to nonclassical monocytes. Notably, sequestering macrophages exhibited a delayed transition from nonclassical monocytes, as evidenced by the persistent expression of Plac8, Treml4, and Ace, which are key genes in the monocyte-to-interstitial macrophage transition. Depletion of monocytes triggered compensatory expansion of lung classical monocytes, which subsequently engaged in nanoplastic uptake. These findings reveal that nanoplastics perturb monocyte-to-macrophage differentiation and reprogram immune dynamics in the lung, implicating immune dysregulation as a potential long-term consequence of environmental nanoplastic exposure.