LAUSR

Epithelial cells form tribological sliding interfaces through the body, often lining tissues and organs, and produce high-water-content mucin gels, thereby protecting underlying cells, tissues, membranes, and organs from damage. Friction and the resulting direct contact shear stresses have been shown to induce the production of pro-inflammatory cytokines and upregulate genes associated with programmed cell death (apoptosis). Using monolayers of immortalized corneal epithelial cells, in situ fluorescence microscopy, and a microtribometer with aqueous gel probes, a series of experiments were performed under acute and chronic conditions to explore onset conditions and progression of apoptosis of these cells. The results reveal that the initiation of apoptosis occurs near physiological shear stresses below 100 Pa. Interesting, the direct contact pressures in the absence of sliding did not initiate apoptosis even at pressures approaching 3 kPa.