Neutrophil transendothelial migration and alteration in vascular permeability: focus on neutrophil-derived azurocidin.

Infiltration and accumulation of polymorphonuclear leukocytes within the tissues is a hallmark of the acute inflammatory response. A prominent feature of acute inflammation is enhanced vascular permeability resulting in edema formation. Such changes in vascular permeability have been known to be dependent upon polymorphonuclear leukocyte interactions with the vascular endothelium.

Neutrophil transepithelial migration: evidence for sequential, contact-dependent signaling events and enhanced paracellular permeability independent of transjunctional migration.

Active migration of polymorphonuclear leukocytes (PMN) through the intestinal crypt epithelium is a hallmark of inflammatory bowel disease and correlates with patient symptoms. Previous in vitro studies have shown that PMN transepithelial migration results in increased epithelial permeability. In this study, we modeled PMN transepithelial migration across T84 monolayers and demonstrated that enhanced paracellular permeability to small solutes occurred in the absence of transepithelial migration but required both PMN contact with the epithelial cell basolateral membrane and a transepithelial chemotactic gradient.