Fatal COVID-19 and Non-COVID-19 Acute Respiratory Distress Syndrome is associated with Incomplete Alveolar Type 1 Epithelial Cell Differentiation from the Transitional State Without Fibrosis

Lung alveolar type-II (AT-II) cells produce pulmonary surfactant (PS), consisting of proteins and lipids. The lipids in PS are primarily responsible for reducing the air-fluid surface tension inside the alveoli of the lungs and to prevent atelectasis. The proteins are of two types: hydrophilic and hydrophobic. Hydrophilic surfactants are primarily responsible for opsonisation, thereby protecting the lungs from microbial and environmental contaminants. Hydrophobic surfactants are primarily responsible for respiratory function. Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) enters the lungs through ACE-2 receptors on lungs and replicates in AT-II cells leading to the etiology of Coronavirus disease – 2019 (COVID-19). The SARS-CoV-2 virus damages the AT-II cells and results in decreased production of PS. The clinical symptoms of acute respiratory distress syndrome (ARDS) in COVID-19 patients are like those of neonatal respiratory distress syndrome (NRDS). The PS treatment is first-line treatment option for NRDS and found to be well tolerated in ARDS patients with inconclusive efficacy. Over the past 70°years, a lot of research is underway to produce natural/synthetic PS and developing systems for delivering PS directly to the lungs, in addition to finding the association between PS levels and respiratory illnesses. In the present COVID-19 pandemic situation, the scientific community all over the world is searching for the effective therapeutic options to improve the clinical outcomes. With a strong scientific and evidence-based background on role of PS in lung homeostasis and infection, few clinical trials were initiated to evaluate the functions of PS in COVID-19. Here, we connect the data on PS with reference to pulmonary physiology and infection with its possible therapeutic benefit in COVID-19 patients.

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Injurious Mechanical Ventilation and End-Organ Epithelial Cell Apoptosis and Organ Dysfunction in an Experimental Model of Acute Respiratory Distress Syndrome

JAMA ◽

10.1001/jama.289.16.2104 ◽

2003 ◽

Vol 289 (16) ◽

pp. 2104 ◽

Cited By ~ 454

Author(s):

Yumiko Imai

Keyword(s):

Mechanical Ventilation ◽

Acute Respiratory Distress Syndrome ◽

Epithelial Cell ◽

Respiratory Distress Syndrome ◽

Respiratory Distress ◽

Experimental Model ◽

Organ Dysfunction ◽

Cell Apoptosis ◽

Distress Syndrome ◽

Epithelial Cell Apoptosis

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Herpes simplex type 1 pneumonitis and acute respiratory distress syndrome in a patient with chronic lymphatic leukemia: a case report

Journal of Medical Case Reports ◽

10.1186/s13256-017-1495-9 ◽

2017 ◽

Vol 11 (1) ◽

Cited By ~ 2

Author(s):

Miriam Luginbuehl ◽

Alexander Imhof ◽

Alexander Klarer

Keyword(s):

Acute Respiratory Distress Syndrome ◽

Case Report ◽

Herpes Simplex ◽

Respiratory Distress Syndrome ◽

Respiratory Distress ◽

Distress Syndrome ◽

Herpes Simplex Type ◽

Chronic Lymphatic Leukemia ◽

Lymphatic Leukemia

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miR-155-5p Promotes Progression of Acute Respiratory Distress Syndrome by Inhibiting Differentiation of Bone Marrow Mesenchymal Stem Cells to Alveolar Type II Epithelial Cells

Medical Science Monitor ◽

10.12659/msm.910316 ◽

2018 ◽

Vol 24 ◽

pp. 4330-4338 ◽

Cited By ~ 6

Author(s):

Jing Jiang ◽

Zhifang Song ◽

Lanyue Zhang

Keyword(s):

Stem Cells ◽

Bone Marrow ◽

Mesenchymal Stem Cells ◽

Acute Respiratory Distress Syndrome ◽

Respiratory Distress Syndrome ◽

Respiratory Distress ◽

Distress Syndrome ◽

Alveolar Type ◽

Type Ii ◽

Marrow Mesenchymal Stem Cells

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Inhibition of CD8+T cells and elimination of myeloid cells by CD4+ Foxp3−T regulatory type 1 cells in acute respiratory distress syndrome

Clinical and Experimental Pharmacology and Physiology ◽

10.1111/1440-1681.12656 ◽

2016 ◽

Vol 43 (12) ◽

pp. 1191-1198 ◽

Cited By ~ 2

Author(s):

Guang-Gang Li ◽

Ying-Hua Cao ◽

Yue Run ◽

Ru-Xiang Xu ◽

Zhen-Dong Zheng

Keyword(s):

T Cells ◽

Acute Respiratory Distress Syndrome ◽

Respiratory Distress Syndrome ◽

Respiratory Distress ◽

Cd8 T Cells ◽

Distress Syndrome ◽

Myeloid Cells ◽

Regulatory Type

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Alveolar Type 2 Epithelial Cells as Potential Therapeutics for Acute Lung Injury/Acute Respiratory Distress Syndrome

Current Pharmaceutical Design ◽

10.2174/1381612825666191204092456 ◽

2020 ◽

Vol 25 (46) ◽

pp. 4877-4882 ◽

Cited By ~ 2

Author(s):

Honglei Zhang ◽

Yong Cui ◽

Zhiyu Zhou ◽

Yan Ding ◽

Hongguang Nie

Keyword(s):

Acute Respiratory Distress Syndrome ◽

Acute Lung Injury ◽

Epithelial Cells ◽

Lung Injury ◽

Respiratory Distress Syndrome ◽

Respiratory Distress ◽

Distress Syndrome ◽

Alveolar Type ◽

Lung Epithelial

: Acute lung injury/acute respiratory distress syndrome is a common clinical illness with high morbidity and mortality, which is still one of the medical problems urgently needed to be solved. Alveolar type 2 epithelial cells are an important component of lung epithelial cells and as a kind of stem cells, they can proliferate and differentiate into alveolar type 1 epithelial cells, thus contributing to lung epithelial repairment. In addition, they synthesize and secrete all components of the surfactant that regulates alveolar surface tension in the lungs. Moreover, alveolar type 2 epithelial cells play an active role in enhancing alveolar fluid clearance and reducing lung inflammation. In recent years, as more advanced approaches appear in the field of stem and progenitor cells in the lung, many preclinical studies have shown that the cell therapy of alveolar type 2 epithelial cells has great potential effects for acute lung injury/acute respiratory distress syndrome. We reviewed the recent progress on the mechanisms of alveolar type 2 epithelial cells involved in the damaged lung repairment, aiming to explore the possible therapeutic targets in acute lung injury/acute respiratory distress syndrome.

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