Interface-level mechanisms of plant protein particles on friction and damage in in vitro biofidelic epithelial models

Epithelial surfaces rely on a mucous layer at contact interfaces to protect against mechanical stresses. Disruption of mucous lubrication compromises its protective function, increasing the exposure and vulnerability of underlying tissues to frictional damage. This study uses a novel biofidelic epithelial model that incorporates living cells, to study the interface-level mechanisms of friction, stress-induced cell membrane rupture and cell detachment in the presence and absence of mucous lubrication. This comprehensive approach bridges the disciplines of cell biology and tribology, offering new insights into particle-mediated lubrication at biological interfaces. This is relevant to understanding the heightened ocular and oral sensations associated with mucous lubrication failure, as seen in dry eye and dry mouth conditions and during oral perception of alternative plant protein ingredients such as fava bean protein isolate (FBPI). Friction experiments and subsequent cell damage analysis revealed that FBPI particles reduced friction by mitigating adhesion forces, while mucous layers further diminish shear-induced damage. In the absence of a mucous layer, stronger adhesive interactions at the cell-probe interface led to increased friction and cellular damage. Cell membrane rupture occurred when mechanical stresses exceeded critical thresholds, whereas detachment resulted from the breaking of fibronectin bonds at cell-fibronectin junctions. These findings highlight interface level mechanisms that can be applied towards the development of alternative food proteins and the further design of biofidelic testbeds.