Abstract

Lung surfactant (LS) is a mixture of lipids and proteins that lines the air-liquid interface of the alveolar walls and modulates the surface tension in the lungs. It therefore greatly reduces the mechanical work of breathing as well as prevents alveolar collapse upon expiration. Blood serum leaking into the alveoli as a result of trauma can lead to LS inhibition, which is one characteristic of acute respiratory distress syndrome (ARDS). The competitive adsorption of serum proteins, such as albumin, to the air-liquid interface of the alveoli blocks LS from forming a functional monolayer during ARDS. The addition of hydrophilic polymers, such as polyethylene glycol and chitosan, to the liquid subphase has been shown to enhance interfacial LS adsorption in vitro. Optimal amounts of polymer allow LS to form a functional monolayer in the presence of albumin, thus reversing inhibition. Albumin must be displaced from the air-liquid interface in order for a functional monolayer of LS to form. Imaging of the competitive adsorption process with confocal microscopy has allowed us to better understand the mechanisms behind forming an interfacial LS monolayer under inhibitory conditions. We can simultaneously track LS, polymer, and albumin, as well as separately visualize phenomena occurring at the interface from those occurring in the bulk. As a result of these capabilities, we have studied how various parameters affect the transport of LS to the interface and the displacement of albumin in order to form a functional surfactant monolayer.

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