CHANGES IN THE CONTENT AND FEATURES OF LOCALIZATION OF ANGIOTENSIN-CONVERTING ENZYME-2 (ACE2) IN ACUTE EXPERIMENTAL BRONCHOPNEUMONIA
D.S. Ziablitsev1, O.O. Dyadik2, A.O. Tikhomirov3, M.M. Tsvetkova1, S.V. Ziablitsev1
- O. Bogomolets National Medical University, Kyiv, Ukraine;
- Shupyk National Healthcare University of Ukraine, Kyiv; 3 Palladin Institute of Biochemistry, National Academy of
Sciences of Ukraine, Kyiv, Ukraine
DOI: https://doi.org/10.15407/fz68.03.024
Abstract
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.
Keywords:
angiotensin-converting enzyme-2 (ACE2); bronchopneumonia; experimental model; inflammation.
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