Biophysical parameters affecting lung surfactant function, surface tension and the transition from aerosol to droplet exhalation (in relation to COVID-19 infection)

Abstract

A considerable number of biophysical and biochemical studies has increased our understanding of the surface activity of surfactant proteins B and C (SP-B, SP-C) in the (mammalian) lung and their importance for a healthy, proper breathing system. For instance, it is well-known that these surfactant proteins are released from the lamellar bodies of type II cells of the lung alveoli (type II pneumocytes), and that at compression, the lipid-protein monolayer of the surfactant is squeezed into three-dimensional (3D) stacks, acting as a surfactant reservoir. Moreover, studies have demonstrated the influence of hydrophobic nanoparticles on lung surfactant model systems, well before the outbreak of the COVID-19 pandemic. The potentially devastating effect of SARS-CoV-2 infection on vital lung function, including pneumonia and Acute respiratory distress syndrome (ARDS), meanwhile has been confirmed worldwide by thousands of fatal cases, although the mechanism of its onset is not completely understood. In theory, any virus carrying palmitoylated spike proteins (like beta-coronaviruses in general) might interfere with the alveolar surface activity, when infecting the deep respiratory system. However, it is clearly established that SARS-CoV-2 uses the Angiotensin converting enzyme 2 receptor (ACE2) for entry in the host, which receptor is expressed on the same type II pneumocytes, and, as a result, the virus may directly interfere with the secretion of surfactant proteins. This study aims at elucidating the main targets for containment of the spread of the SARS-CoV-2 virus via the respiratory system, a better understanding of the role of virus-surfactant interactions, the formation of aerosols and role of the inflammatory components of the immune system, as well as the role of positive pressure ventilation systems on particle exhalation, as being used at ICUs. Finally, suggestions are made for important goals for future biophysics research in infectious disease prevention and containment.

Type 2 alveolar epithelial cell-derived circulating extracellular vesicle-encapsulated surfactant protein C as a mediator of cardiac inflammation in COVID-19

“…Consisting of hydrophobic lipid components as well, lung surfactant could also enhance the pathogenesis of COVID-19 by acting as a site for accumulation of SARS-CoV-2 particles [ 3 ], as the virus was recently reported to become lipid-soluble upon palmitoylation of its spike protein, which appears to be a prerequisite for successful entry of the virus into potential host cells [ 4 ].…”