Induction of Inflammatory Responses in Human Bronchial Epithelial Cells by Pb2+-Containing Model PM2.5 Particles via Downregulation of a Novel Long Noncoding RNA lnc-PCK1-2:1

Airborne particular matter (PM 2.5 ) contains complex mixtures of pollutants, and their compositions also vary with time and location. Inhalation of PM 2.5 may cause a number of diseases, such as bronchial and lung inflammation and lung cancer. So far, how different components of PM 2.5 contribute to inflammation and toxicity is still not known. To identify key PM 2.5 components that are responsible for inflammation, here we took a reductionism approach and synthesized a model PM 2.5 library containing 20 carbon nanoparticle based members with loadings of As(III), Pb 2+, Cr(VI), and BaP individually or in combination at environment relevant concentrations. We discovered that only carbon nanoparticle–Pb 2+ adducts, not other pollutants or adducts, induced inflammation in human bronchial cells by suppressing the expression of a novel long noncoding RNA lnc-PCK1-2:1, while lnc-PCK1-2:1 routinely plays a regulatory role in inhibiting inflammation. This finding was further substantiated by varying Pb 2+ loadings on carbon nanoparticles and overexpressing lnc-PCK1-2:1 . The success of this approach opens an avenue for further elucidation of molecular mechanisms of PM 2.5 -induced inflammation and toxicity.