Acute respiratory distress syndrome (ARDS) is a pulmonary disease that affects over 300,000 people in the US each year and has a mortality rate of 40%. Patients with COVID-19 viral infections also commonly develop ARDS, both concurrently with the infection and with a delayed onset. A major barrier for the effective treatment of ARDS is that the underlying causes of the disease are poorly understood. We believe that the root cause may be a change in the interfacial properties of the lung surfactant due to blood components, in particular phospholipase A2, entering the lungs as a result of inflammation. PLA2 catalyzes the formation of soluble lysolipids from phospholipids in the membranes of bacteria or viruses. We hypothesize that the increased lysolipid concentrations following inflammation decrease the dilatational modulus, causing uneven lung inflation. A combined confocal microscope/capillary pressure microtensiometer (CFM/CPM) has been developed to create curved air water interfaces on the scale of the alveoli, to study surfactant adsorption and desorption and the dilatational properties while simultaneously visualizing the lung surfactant monolayer morphology with confocal microscopy.
We present a study of static and dynamic interfacial properties and morphologies using both clinical replacement lung surfactants relevant to ARDS treatment and simple model lung surfactants made of phospholipids and lung surfactant proteins. We challenge lung surfactant covered interfaces with chemical species that arise from inflammation, such as lysolipid (lysoPC) to determine any changes in interfacial morphology and dynamic properties in an environment that could arise in ARDS. The combined CFM/CPM can be used to measure surface tension and surface dilatational modulus at normal breathing frequencies and relate monolayer dynamics directly to the morphological structures on the interface during adsorption, oscillation, and introduction of lysoPC.