Journal
PHYSIOLOGICAL RESEARCH
Volume 70, Issue -, Pages S195-S208Publisher
ACAD SCIENCES CZECH REPUBLIC, INST PHYSIOLOGY
DOI: 10.33549/physiolres.934763
Keywords
Pulmonary surfactant; Alveolar type II cell; SARS-CoV-2; COVID-19; ARDS
Categories
Funding
- [VEGA 1/0055/19]
- [VEGA 1/0004/21]
- [APVV-17-0250]
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This review highlights the key role of alveolar type II cells and reduced surfactant in the pathogenesis of respiratory form of COVID-19, emphasizing the rational basis for exogenous surfactant therapy in COVID-19 ARDS patients.
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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