Preventive approach against drug-induced pulmonary fibrosis through the suppression of epithelial-mesenchymal transition

A number of drugs induce pulmonary injury and subsequently lead to serious lung diseases such as pulmonaryfibrosis as the adverse drug reactions. However, an effective preventive approach against drug-induced pulmonary fibrosishas not been established due to poor understanding of common preventive targets in a variety of drugs showing pulmonarytoxicity. Epithelial-mesenchymal transition (EMT), a cellular phenotypic change of the epithelial to mesenchymal state,contributes to the development of pulmonary fibrosis through the conversion of damaged alveolar epithelium intomyofibroblasts. As several drugs with pulmonary toxicity have been reported to induce EMT, EMT serves as a bridgebetween the drugs and pulmonary fibrosis. Accumulated evidence supports the potential of EMT as a preventive targetagainst drug-induced pulmonary fibrosis. Additionally, since there are mechanistic differences between the mainpharmacological effect and EMT induced by the drug, prevention based on EMT suppression would be possible andwould contribute to continuous clinical treatment with the drug to avoid EMT-mediated serious pulmonary fibrosis.Furthermore, targeting EMT seems to be adequate for exerting a preventive effect since EMT in damaged alveolarepithelial cells occurs prior to the development of the pathophysiological state of the whole lung in a bleomycin-inducedlung injury rat model. This viewpoint deals with the benefits and perspectives of preventive approaches against druginduced pulmonary fibrosis through the suppression of EMT, which has rarely been addressed.     

Electron microscopic time‐lapse visualization of surface pore filtration on particulate matter trapping process

A scanning electron microscope (SEM) was used to dynamically visualize the particulate matter (PM) trapping process on diesel particulate filter (DPF) walls at a micro scale as ‘time‐lapse’ images corresponding to the increase in pressure drop simultaneously measured through the DPF. This visualization and pressure drop measurement led to the conclusion that the PM trapping in surface pores was driven by PM bridging and stacking at constricted areas in porous channels. This caused a drastic increase in the pressure drop during PM accumulation at the beginning of the PM trapping process. The relationship between the porous structure of the DPF and the depth of the surface pore was investigated in terms of the porosity distribution and PM penetration depth near the wall surface with respect to depth. The pressure drop calculated with an assumed surface pore depth showed a good correspondence to the measured pressure drop.