We recently described a murine asthma model with strong evidence for PM-mediated vascular barrier dysfunction with increased protein leakage into bronchoalveolar lavage (BAL), a marker of acute inflammatory lung damage [12] . By assessment of direct effects on endothelial barrier integrity in vitro, we further demonstrated that the vascular hyperpermeability mediated by intratracheal PM exposure is mainly dependent on acute endothelial barrier disruption by PM [13] . Exposure of human lung EC to PM resulted in significant ROS generation, which mediates p38beta MAPK activation, leading to the phosphorylation of HSP27 [13] . Phosphorylated HSP27 facilitates the synthesis of stress fibers and formation of paracellular gaps, which causes protein-containing fluid to leak from the microvessel lumen to the lung alveoli, leading to further pulmonary inflammation [13] . However, these previous findings did not explain the persistent character of PM-mediated endothelial barrier disruption.