Coronavirus (SARS-CoV-2) enters the cell by binding to a transmembrane glycoprotein, angiotensin-converting enzyme-2 (ACE2), which is expressed on the surface of the bronchial and alveolar epithelium. In this regard, the aim of this study was to determine changes in the content and characteristics of tissue localization of ACE2 in the model of acute bronchopulmonary inflammation. The latter was modeled by endotracheal injection of a foreign body (Capron thread) and a solution of lipopolysaccharide (LPS; 50 μl at a dose of 12.5 mg/kg) against the background of systemic administration of LPS for two days before surgery (250 mg/ kg). ACE2 localization and quantity were evaluated by immunohistochemical and western blot assays with the use of a specific monoclonal antibody. The experiment reproduced acute exudative-hemorrhagic bronchopneumonia with the development of diffuse progressive pulmonary fibrosis with lethality in 36% of animals. Acute exudative inflammation was accompanied by complete inhibition of ACE2 expression in bronchial epitheliocytes and its significant decrease in alveolocytes type II. With the development of the proliferative stage of bronchopneumonia, the level of ACE2 was restored, subsequently remaining without significant changes. The obtained experimental data suggest the existence of a relationship between the features of quantitative changes in the ACE2 level in the bronchopulmonary epithelium and the undulating course of the inflammatory process during SARS-CoV-2 infection.