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Phospholipids are found throughout the natural world, including the lung surfactant (LS) layer that reduces pulmonary surface tension and enables breathing. Fibrinogen, a protein involved in the blood clotting process, is implicated in LS inactivation and the progression of disorders such as acute respiratory distress syndrome. However, the interaction between fibrinogen and LS at the air–water interface is poorly understood. Through a combined microrheological, confocal and epifluorescence microscopy approach we quantify the interfacial shear response and directly image the morphological evolution when a model LS monolayer is penetrated by fibrinogen. When injected into the subphase beneath a monolayer of the phospholipid dipalmitoylphosphatidylcholine (DPPC, the majority component of LS), fibrinogen preferentially penetrates disordered liquid expanded (LE) regions and accumulates on the boundaries between LE DPPC and liquid condensed (LC) DPPC domains. Thus, fibrinogen is line active. Aggregates grow from the LC domain boundaries, ultimately forming a percolating network. This network stiffens the interface compared to pure DPPC and imparts the penetrated monolayer with a viscoelastic character reminiscent of a weak gel. When the DPPC monolayer is initially compressed beyond LE–LC coexistence, stiffening is significantly more modest and the penetrated monolayer retains a viscous-dominated, DPPC-like character. 

Microbutton rheometry reveals that the chiral morphology of dipalmitoylphosphatidylcholine (DPPC) monolayers imparts a chiral nonlinear rheological response. The nonlinear elastic modulus and yield stress of DPPC monolayers are greater when sheared clockwise (C), against the natural winding direction of DPPC domains, than counter-clockwise (CC). Under strong CC shear strains, domains deform plastically; by contrast, domains appear to fracture under strong C shearing. After CC shearing, extended LC domains develop regular patterns of new invaginations as they recoil, which we hypothesize reflect the nucleation and growth of new defect lines across which the tilt direction undergoes a step change in orientation. The regular spacing of these twist-gradient defects is likely set by a competition between the molecular chirality and the correlation length of the DPPC lattice. The macroscopic mechanical consequences of DPPC's underlying molecular chirality are remarkable, given the single-component, non-cross-linked nature of the monolayers they form.