Abstract: Exposure to widely used inert fibrous nanomaterials (e.g., glass fibers, carbon nanotubes) might result in asbestos-like lung pathologies, becoming an important environmental and health concern. However, the origin of the pathogenesis of such fibers has not yet been clearly established. Here, we report on an electrochemical nanosensor which is used to monitor and quantitatively characterize the flux and dynamics of reactive species release during the progress of frustrated phagocytosis of glass nanofibers by single macrophages. We show the existence of an intense prolonged release of reactive oxygen and nitrogen species (ROS/RNS) by single macrophages at the level of their phagocytic cups. This continued massive ROS and RNS leakage damages peripheral cells and eventually translates into chronic inflammation and lung injury, as seen in in vitro co-culture and in vivo experiments.

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DOI: 10.1038/s41565-023-01575-0