PMN transmigration across intestinal epithelia and into crypt lumens is a hallmark of active intestinal disease. Models of the transmigratory event indicate that movement of PMN across intercellular tight junctions transiently increases junctional permeability, thus decreasing epithelial barrier function. Once accumulated in the lumen, activated PMN may release unidentified mediators which activate the epithelial transport mechanisms responsible for secretory diarrhea. Further characterization of such epithelial-PMN interactions may allow identification of rational treatment strategies aimed at intervening in the epithelial dysfunction characterizing this type of cell-cell interaction.