Alexandra Farrell

Lung surfactant (LS) is a lipid-protein mixture lining the air-water interface in lung alveoli that facilitates breathing. Acute respiratory distress syndrome (ARDS) is a potentially fatal breathing complication caused by trauma with the physical manifestations involving distended alveoli, alveolar flooding, among others. An understanding of the role of LS in the progression of ARDS is pivotal in developing a cure for the disease. LS ensures uniform lung inflation and prevents lung collapse. Dipalmitoylphosphatidylcholine (DPPC) is a LS that is largely responsible for keeping lungs stable and non-collapsing. Mechanically, lung collapse can be prevented if the alveolar interface has a high enough “interfacial resistance” to dilatational deformation. The dilatational modulus measures this “interfacial resistance”, relating the change in surface tension to change in the interfacial area when an interface undergoes such dilatational deformation at a frequency. This elasticity is likely compromised during ARDS, in which the dilatational modulus of the alveolar interface decreases significantly, causing a breathing complication called the “Laplace Instability”. Lysolipids (LPC) are an inflammatory product that results from lung trauma such as car accidents, pneumonia (as with Covid-19), etc. Addition of LPC can cause desorption of DPPC (and other LS lipids), with behavior mimicking that of pure LPC, and causing a reduced dilatational modulus and the subsequent Laplace Instability. In our experiment using Langmuir trough, we showed that there is a time and concentration dependence of this phenomenon. This observation allows us to gain a better understanding of the role of inflammatory products in ARDS progression.