Inhaled nanoparticles (< 100 nm) reaching the deep lung region first interact with the pulmonary surfactant, a thin lipid film lining the alveolar epithelium. To date, most biophysical studies have focused on particle induced modifications of the film interfacial properties. In comparison, there is less work on the surfactant bulk properties, and on their changes upon particle exposure. Here we study the viscoelastic properties of a biomimetic pulmonary surfactant in the presence of various engineered nanoparticles. The microrheology technique used is based on the remote actuation of micron-sized wires via the application of a rotating magnetic field and on timelapse optical microscopy. It is found that particles strongly interacting with lipid vesicles, such as cationic silica (SiO2, 42 nm) and alumina (Al2O3, 40 nm) induce profound modifications of the surfactant flow properties, even at low concentrations. In particular, we find that silica causes fluidification, while alumina induces a liquid-to-soft solid transition. Both phenomena are described quantitatively and accounted for in the context of colloidal physics models. It is finally suggested that the structure and viscosity changes could impair the fluid reorganization and recirculation occurring during breathing.

Single molecule mechanics of poly(styrene) polymer chains is investigated in different organic solvents with atomic force microscopy (AFM). The acquired force−extension profiles can be well fitted with a modified freely jointed chain (FJC) model. The model describes the force−extension profiles in terms of an apparent Kuhn length and an elasticity constant. The elasticity constant is found to be the same for all different solvents investigated. Best fit of the force−extension profiles with the FJC model reveals that the Kuhn length varies systematically with solvent quality. In fact, one can establish a good correlation between the Kuhn length and the Flory−Huggins interaction parameter. The increase in the Kuhn length with increasing solvent quality reflects the larger extent of swelling of the polymer in good solvents.

We report on the development of a new model of alveolar air-tissue interface on a chip. The model consists of an array of suspended hexagonal monolayers of gelatin nanofibers supported by microframes and a microfluidic device for the patch integration. The suspended monolayers are deformed to a central displacement of 40 -80 µm at the air-liquid interface by application of air pressure in the range of 200 -1000 Pa. With respect to the diameter of the monolayers that is 500 µm, this displacement corresponds to a linear strain of 2 -10% in agreement with the physiological strain range in the lung alveoli. The culture of A549 cells on the monolayers for an incubation time 1 -3 days showed viability in the model. We exerted a periodic strain of 5% at a frequency of 0.2 Hz during 1 hour to the cells. We found that the cells were strongly coupled to the nanofibers, but the strain reduced the coupling and induced remodeling of the actin cytoskeleton, which led to a better tissue formation. Our model can serve as a versatile tool in lung investigations such as in inhalation toxicology and therapy.