Abstract
Particulate matters (PMs), represented by PM2.5, are known to aggravate various respiratory diseases such as chronic obstructive pulmonary disease (COPD) and bronchial asthma. Several epidemiological reports have shown that PMs increase the incidence of the onset of coronavirus disease 2019 (COVID-19), which has recently been raging around the world. However, the detailed mechanisms by which PM affects biological systems and triggers the onset of COVID-19 are not clear. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) invades host cells using angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2) expressed on the host cell membrane. Thus, variations in their expression and function are expected to be associated with the pathogenesis of COVID-19. In this study, we aimed to elucidate molecular mechanisms by which PMs affect the onset of COVID-19 by evaluating the expression of ACE2 and TMPRSS2 upon exposure to various PMs. Here we focused on different types of PM such as PM2.5 collected from ambient atmospheres, diesel exhaust particles, titanium dioxide nanoparticles, and Asian sand dust. We introduce the results of the evaluation of the expression level of ACE2 and TMPRSS2, the identification of their expressing cell types in the lung, and the variation in their functions when these PMs were exposed to mouse and human alveolar epithelial cell lines.
