Alveolar type II cells and pulmonary surfactant in COVID-19 era.
A Calkovska, M Kolomaznik, V Calkovsky
Author Information
A Calkovska: Department of Physiology, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava, Martin, Slovak Republic; Clinic of Otorhinolaryngology and Head and Neck Surgery, Jessenius Faculty of Medicine, Comenius University, University Hospital Martin, Martin, Slovak Republic. vladimir.calkovsky@uniba.sk.
中文译文
English
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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Alveolar Epithelial Cells
Angiotensin-Converting Enzyme 2
Animals
COVID-19
Host-Pathogen Interactions
Humans
Lung
Pulmonary Surfactant-Associated Proteins
Pulmonary Surfactants
Receptors, Virus
SARS-CoV-2
Serine Endopeptidases
Virus Internalization
COVID-19 Drug Treatment
Pulmonary Surfactant-Associated Proteins
Pulmonary Surfactants
Receptors, Virus
ACE2 protein, human
Angiotensin-Converting Enzyme 2
Serine Endopeptidases
TMPRSS2 protein, human