Airway epithelial cells, which synthesize and secrete inflammatory and fibrotic mediators, are exposed to mechanical stresses during bronchoconstriction. Because the deformations of the airway wall are transmitted to the airway epithelial cells via cell-cell and cell-matrix attachments, we investigated whether protein production is regulated by stresses applied directly to cell adhesion molecules. Mechanical stresses were applied to RGD and collagen coated beads bound to normal human bronchial epithelial cells using an adaptation of a previously described magnetic twisting device (1). Continuous stress resulted in increased Egr-1 protein at 30 minutes relative to cells with no beads, and cells with beads that were not stressed. Exposure of cells to both collagen and RGD coated beads decreased fibronectin protein at 24 hours, an effect that was partially (collagen) or totally (RGD) negated by 4 hours of continuous exposure to mechanical force. These preliminary results indicate the important role that the extracellular matrix, and forces transmitted via the extracellular matrix, may play in protein production in the normal and asthmatic airway.