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Updated: Aug 1, 2025
Characterization of Immune Cells and Proinflammatory Mediators in the Pulmonary Environment
Published on: June 24, 2020
Lung Expression of Macrophage Markers CD68 and CD163, Angiotensin Converting Enzyme 2 (ACE2), and Caspase-3 in
Denis S Ziablitsev1, Marko Kozyk2, Kateryna Strubchevska2
1Department of Pathophysiology, Bogomolets National Medical University, 01601 Kyiv, Ukraine.
Abstract:
Background and Objectives: The coronavirus (SARS-CoV-2) damages all systems and organs. Yet, to a greater extent, the lungs are particularly involved, due to the formation of diffuse exudative inflammation in the form of acute respiratory distress syndrome (ARDS) with next progression to pulmonary fibrosis. SARS-associated lung damage is accompanied by the pronounced activation of mononuclear cells, damage of the alveoli and microvessels, and the development of organized pneumonia. To study the expression of macrophage markers (CD68 and CD163), angiotensin-converting enzyme-2 (ACE2), and caspase-3 on the results of two fatal clinical observations of COVID-19. Materials and Methods: In both clinical cases, the female patients died from complications of confirmed COVID-19. Conventional morphological and immunohistochemical methods were used. Results: There was an acute exudative hemorrhagic pneumonia with the formation of hyaline membranes, focal organization of fibrin, stromal sclerosis, stasis, and thrombus formation in the lung vessels. Signs such as the formation of hyaline membranes, organization, and fibrosis were more pronounced in severe disease activity. The activation of CD68+/CD163+ macrophages could cause cell damage at an early stage of pneumonia development, and subsequently cause fibrotic changes in lung tissue. ACE2 expression in lung tissue was not detected in severe pneumonia, while in moderate pneumonia, weak expression was noted in individual cells of the alveolar epithelium and vascular endothelium. Conclusions: This finding could show the dependence of ACE2 expression on the severity of the inflammatory process in the lungs. The expression of caspase-3 was more pronounced in severe pneumonia.
Insights
Severe COVID-19 lung damage involves inflammation, fibrosis, and macrophage activation. Angiotensin-converting enzyme-2 (ACE2) expression decreased with disease severity, while caspase-3 increased, indicating its role in severe pneumonia.
Area of Science:
- Pathology
- Immunology
- Pulmonology
Background:
- Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes widespread organ damage, particularly affecting the lungs.
- Lung damage manifests as acute respiratory distress syndrome (ARDS), progressing to pulmonary fibrosis, with associated mononuclear cell activation and organized pneumonia.
Purpose of the Study:
- To investigate the expression of macrophage markers (CD68, CD163), ACE2, and caspase-3 in fatal COVID-19 cases.
- To correlate these markers with the severity of lung pathology in COVID-19.
Main Methods:
- Analysis of lung tissue from two fatal COVID-19 cases.
- Utilized conventional morphological and immunohistochemical techniques.
Main Results:
- Observed acute exudative hemorrhagic pneumonia with hyaline membranes, fibrin organization, sclerosis, stasis, and vascular thrombi.
- Macrophage activation (CD68+/CD163+) correlated with early cell damage and subsequent fibrosis.
- ACE2 expression was absent in severe pneumonia but weakly present in moderate cases; caspase-3 expression was higher in severe pneumonia.
Conclusions:
- ACE2 expression in lung tissue appears inversely related to the severity of the inflammatory process in COVID-19.
- Caspase-3 expression is significantly elevated in severe COVID-19 pneumonia, suggesting its role in disease progression.
