Claudins are the most important components of the tight junctions at the interface of the basolateral and apical membranes of polarized epithelial and endothelial cells. They determine the barrier properties of cell–cell contact existing between two neighboring cells and regulate paracellular permeability. Although maintenance of barrier properties requires intact epithelial tight junctions, relatively little is known about the role of claudins expressed in the alveolar epithelium in the regulation of epithelial permeability in response to inflammatory stimuli and oxidative stress, or injury. The present study was undertaken to determine whether differential expression of tight junction claudins is a mechanism for regulation of oxidant-induced pulmonary epithelial hyperpermeability. Here, we show that claudin-2 plays an important role in the regulation of epithelial barrier function during oxidative stress.
