Exposure to particulate matter upregulates ACE2 and TMPRSS2 expression in the murine lung

Coronavirus including particulate matter (PM), as a risk factor for COVID-19 infection and severity of illness, in addition to numerous factors such as pre-existing conditions, aging and smoking. However, the mechanisms by which air pollution is involved in the manifestation and/or progression of COVID-19 is still unknown. In this study, we used a mouse model exposed to crude PM, collected by the cyclone method, to evaluate the pulmonary expression of angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine type 2 (TMPRSS2), the two molecules required for the entry of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) into host cells. Multiplex immunohistochemical analysis revealed that exposure to PM increased the expression of these two molecules at the same site. Furthermore, image cytometry analysis revealed increased expression of these proteins, particularly, in the alveolar type 2 cells and macrophages, which are potential targets for SARSCoV-2. Our findings provide an experimental mediated by the impact of SARS-CoV-2 on the site of entry. The study results suggest that examining these effects might help to advance our understanding of COVID-19 and aid the development of appropriate social interventions.

Automated summary

The study used a mouse model exposed to particulate matter to evaluate the increased expression of ACE2 and TMPRSS2 in the lungs, which are required for the entry of SARS-CoV-2. The findings suggest that particulate matter may enhance the expression of these proteins in alveolar type 2 cells and macrophages, potentially making them targets for SARS-CoV-2. This research provides insight into how air pollution could influence the severity of COVID-19 infection.