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Alveolar type II cells and pulmonary surfactant in COVID-19 era
A. Calkovska, M. Kolomaznik, V. Calkovsky
Language English Country Czech Republic
Document type Journal Article, Review
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- MeSH
- Angiotensin-Converting Enzyme 2 metabolism MeSH
- COVID-19 immunology metabolism virology MeSH
- COVID-19 Drug Treatment MeSH
- Host-Pathogen Interactions MeSH
- Virus Internalization MeSH
- Humans MeSH
- Lung drug effects immunology metabolism virology MeSH
- Pulmonary Surfactants therapeutic use MeSH
- Alveolar Epithelial Cells drug effects immunology metabolism virology MeSH
- Pulmonary Surfactant-Associated Proteins metabolism MeSH
- SARS-CoV-2 immunology pathogenicity MeSH
- Serine Endopeptidases metabolism MeSH
- Receptors, Virus metabolism MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Review MeSH
In this review, we discuss the role of pulmonary surfactant in the host defense against respiratory pathogens, including novel coronavirus SARS-CoV-2. In the lower respiratory system, the virus uses angiotensin-converting enzyme 2 (ACE2) receptor in conjunction with serine protease TMPRSS2, expressed by alveolar type II (ATII) cells as one of the SARS-CoV-2 target cells, to enter. ATII cells are the main source of surfactant. After their infection and the resulting damage, the consequences may be severe and may include injury to the alveolar-capillary barrier, lung edema, inflammation, ineffective gas exchange, impaired lung mechanics and reduced oxygenation, which resembles acute respiratory distress syndrome (ARDS) of other etiology. The aim of this review is to highlight the key role of ATII cells and reduced surfactant in the pathogenesis of the respiratory form of COVID-19 and to emphasize the rational basis for exogenous surfactant therapy in COVID-19 ARDS patients.
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