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Review
. 2023 Aug 31;43(8):BSR20230504.
doi: 10.1042/BSR20230504.

Surfactant replacement therapy as promising treatment for COVID-19: an updated narrative review

Khaled Khudadah #  1 , Alaa Ramadan #  2 , Ahmed Othman #  1 , Neveen Refaey  3 , Amr Elrosasy  4 , Ayoub Rezkallah  5   6 , Toka Heseba  7 , Mostafa Hossam El Din Moawad  8   9 , Ammar Mektebi  10 , Sewar A Elejla  11 , Mohamed Abouzid  12   13 , Basel Abdelazeem  14   15
Affiliations
Review

Surfactant replacement therapy as promising treatment for COVID-19: an updated narrative review

Khaled Khudadah et al. Biosci Rep. .

Abstract

Patients with COVID-19 exhibit similar symptoms to neonatal respiratory distress syndrome. SARS-CoV-2 spike protein has been shown to target alveolar type 2 lung cells which synthesize and secrete endogenous surfactants leading to acute respiratory distress syndrome in some patients. This was proven by post-mortem histopathological findings revealing desquamated alveolar type 2 cells. Surfactant use in patients with COVID-19 respiratory distress syndrome results in marked improvement in respiratory parameters but not mortality which needs further clinical trials comparing surfactant formulas and modes of administration to decrease the mortality. In addition, surfactants could be a promising vehicle for specific drug delivery as a liposomal carrier, which requires more and more challenging efforts. In this review, we highlight the current reviews and two clinical trials on exogenous surfactant therapy in COVID-19-associated respiratory distress in adults, and how surfactant could be a promising drug to help fight the COVID-19 infection.

Keywords: Acute respiratory distress syndrome; Alveolar cells type 2; COVID-19; SARS-CoV-2; pulmonary surfactant.

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Conflict of interest statement

The authors declare that there are no competing interests associated with the manuscript.

Figures

Figure 1
Figure 1. Structure of SARS-CoV-2 and methods for entrance into host cells
The nucleocapsid, membrane, envelope, and spike protein are the four structural proteins that are encoded by the single-stranded RNA viral genome. Both options for viral internalization—via direct fusion of the viral envelope and the host cell plasma membrane or—via endocytic entry, followed by fusion between the viral envelope and the endosomal membrane—are triggered by the binding of Si of the viral spike protein to the ACE-2 receptor on host cells. Abbreviations: ACE-2, angiotensin-converting enzyme 2; SARS-CoV-2, severe acute respiratory syndrome coronavirus-Z; TMPRSS2, transmembrane protease serine 2, subunits 1, 2, and 2. From ‘Mechanisms of SARS-CoV-2 Viral Entry,’ modified, by BioRender.com (2021). Retrieved from https://app.biorender.com/biorender-templates.
Figure 2
Figure 2. COVID-19-related acute respiratory distress syndrome: 1-Cytokine storm 2- neutrophil degranulation and serum leak 3- pneumocyte destruction
Retrieved from https://app.biorender.com/biorender-templates.
Figure 3
Figure 3. Effect of exogenous pulmonary surfactant therapy
Figure 4
Figure 4. Surfactant replacement therapy showing improved oxygenation and decreased serum leak: I, the restoration of the surfactant layer. II, neutrophil recruitment. III, the neutralization of COVID-19 virus by proteins A and D. IV, recovered surfactant layer
Figure 5
Figure 5. The diagrammatic renderings of the preventative and ( A) therapeutic applications of surfactants against COVID-19 The prevention of COVID-19 by a surfactant-based gargle, (B) the entry of the SARS-CoV-2 virus into the lung alveoli, and (C) the effect of surfactant in circulation
The surfactant either covers the virus and makes it inactive or inactivates it.
See this image and copyright information in PMC

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