Alveolar Type II Cells and Pulmonary Surfactant in COVID-19 Era

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, expresse...

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Bibliographic Details
Published in:Physiological research 2021, Vol.70 (Suppl 2), p.S195-S208
Main Authors: CALKOVSKA, A, KOLOMAZNIK, M, CALKOVSKY, V
Format: Article
Language:English
Subjects:
ACE2
Alveoli
Angiotensin
Angiotensin-converting enzyme 2
Coronaviruses
COVID-19
Edema
Etiology
Gas exchange
Lipids
Oxygenation
Peptidyl-dipeptidase A
Respiratory diseases
Respiratory distress syndrome
Respiratory system
Review
Serine proteinase
Severe acute respiratory syndrome coronavirus 2
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Summary: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.
ISSN:0862-8408
1802-9973
DOI:10.33549/physiolres.934763