From coffee beans flowing in a chute to cells remodelling in a living tissue, a wide variety of close-packed collective systems— both inert and living—have the potential to jam. The collective can sometimes flow like a fluid or jam and rigidify like a solid. The unjammed-to-jammed transition remains poorly understood, however, and structural properties characterizing these phases remain unknown. Using primary human bronchial epithelial cells, we show that the jamming transition in asthma is linked to cell shape, thus establishing in that system a structural criterion for cell jamming. Surprisingly, the collapse of critical scaling predicts a counter-intuitive relationship between jamming, cell shape and cell–cell adhesive stresses that is borne out by direct experimental observations. Cell shape thus provides a rigorous structural signature for classification and investigation of bronchial epithelial layer jamming in asthma, and potentially in any process in disease or development in which epithelial dynamics play a prominent role.

Coordinated motions of close-packed multicellular systems typically generate cooperative packs, swirls, and clusters. These cooperative motions are driven by active cellular forces, but the physical nature of these forces and how they generate collective cellular motion remain poorly understood. Here, we study forces and motions in a confined epithelial monolayer and make two experimental observations: 1) the direction of local cellular motion deviates systematically from the direction of the local traction exerted by each cell upon its substrate; and 2) oscillating waves of cellular motion arise spontaneously. Based on these observations, we propose a theory that connects forces and motions using two internal state variables, one of which generates an effective cellular polarization, and the other, through contractile forces, an effective cellular inertia. In agreement with theoretical predictions, drugs that inhibit contractility reduce both the cellular effective elastic modulus and the frequency of oscillations. Together, theory and experiment provide evidence suggesting that collective cellular motion is driven by at least two internal variables that serve to sustain waves and to polarize local cellular traction in a direction that deviates systematically from local cellular velocity.

Biological cells sense and respond to mechanical forces, but how such a mechanosensing process takes place in a nonlinear inhomogeneous fibrous matrix remains unknown. We show that cells in a fibrous matrix induce deformation fields that propagate over a longer range than predicted by linear elasticity. Synthetic, linear elastic hydrogels used in many mechanotransduction studies fail to capture this effect. We develop a nonlinear microstructural finite-element model for a fibre network to simulate localized deformations induced by cells. The model captures measured cell-induced matrix displacements from experiments and identifies an important mechanism for long-range cell mechanosensing: loss of compression stiffness owing to microbuckling of individual fibres. We show evidence that cells sense each other through the formation of localized intercellular bands of tensile deformations caused by this mechanism.

Atomic force microscopy (AFM) is a powerful tool for studying tribology (adhesion, friction, and lubrication) at the nanoscale and is emerging as a critical tool for nanomanufacturing. However, nanoscale wear is a key limitation of conventional AFM probes that are made of silicon and silicon nitride (SiNx). Here we present a method for systematically quantifying tip wear, which consists of sequential contact-mode AFM scans on ultrananocrystalline diamond surfaces with intermittent measurements of the tip properties using blind reconstruction, adhesion force measurements, and transmission electron microscopy (TEM). We demonstrate direct measurement of volume loss over the wear test and agreement between blind reconstruction and TEM imaging. The geometries of various types of tips were monitored over a scanning distance of approximately 100 mm. The results show multiple failure mechanisms for different materials, including nanoscale fracture of a monolithic Si tip upon initial engagement with the surface, film failure of a SiNx-coated Si tip, and gradual, progressive wear of monolithic SiNx tips consistent with atom-by-atom attrition. Overall, the method provides a quantitative and systematic process for examining tip degradation and nanoscale wear, and the experimental results illustrate the multiple mechanisms that may lead to tip failure.