Inhalable pollutants can cross the alveolar-capillary barrier into the bloodstream, and pollutant-elicited oxidative stress at this barrier is a well-recognized pathogenic driver of systemic diseases. However, direct quantification of oxidative stress at the dynamic alveolar-capillary barrier has remained unattainable due to the lack of sensing tools, substantially limiting our understanding of pollutant toxicology and associated pathogenesis. Herein, we develop nanomesh bioelectronics that simultaneously function as a basement membrane analogue and an electrochemical sensor. The bioelectronic interface recapitulates the native basement membrane’s nanofibrous architecture, ultrathin geometry, high permeability, and mechanical properties, while exhibiting stable electrochemical responses to H2O2 under cyclic stretching. When incorporated into lung-on-a-chip, the bioelectronics enable simultaneous reconstruction of the alveolar-capillary barrier and in situ quantification of oxidative stress during respiratory stretching. Using benzo[a]pyrene as a model carcinogenic pollutant, we uncover a biphasic regulatory role of vascular endothelium: an intact endothelium reinforces epithelial resistance to pollutant stimuli, whereas endothelial dysfunction converts protective crosstalk into pathological oxidative amplification. Rat models further confirm that systemic vascular health shapes pulmonary responses to environmental insults. The proposed bioelectronics provide a versatile tool for engineering biological barriers and dissecting intercompartmental crosstalk.
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Zhao et al. (2026) studied this question.
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