Peripheral alveolar macrophages express more ACE2 immunoreactivity than in hilar area in human autopsied lung.

OBJECTIVE

SARS-coronavirus 2 (SARS-CoV-2) is the cause of the coronavirus disease 19 (COVID-19). SARS-CoV-2 spike (S) glycoprotein binds to a cellular receptor angiotensin converting enzyme 2 (ACE2). COVID-19 pneumonia has a tendency to cause peripheral inflammation. To test the possibility that peripheral predominance of COVID-19 pneumonia is dependent on the peripheral expressions of ACE2, ACE2-positive macrophages and type 2 alveolar epithelial cells were immunohistochemically counted under the microscope, and compared between peripheral and hilar lung areas.

RESULTS

Our result shows that peripheral alveolar macrophages express statistically significantly higher positivity in ACE2 than hilar alveolar macrophages. On the other hand, no statistically significant difference is shown in the expression of ACE2 in type 2 alveolar epithelia between peripheral and hilar alveoli. The higher expression of ACE2 immunoreactivity in peripheral alveolar macrophages may contribute to understanding the peripheral susceptibility of COVID-19 pneumonia.