Laroux F S, Lefer D J, Kawachi S, Scalia R, Cockrell A S, Gray L, Van der Heyde H, Hoffman J M, Grisham M B
Department of Molecular and Cellular Physiology, LSU Health Sciences Center, Shreveport, LA 71130, USA.
Antioxid Redox Signal. 2000 Fall;2(3):391-6. doi: 10.1089/15230860050192161.
Recent studies by a number of different laboratories have implicated nitric oxide (NO) as an important modulator of a variety of acute and chronic inflammatory disorders. A hallmark of inflammation is the adhesion of leukocytes to post-capillary venular endothelium and the infiltration of leukocytes into the tissue interstitium. Leukocyte adhesion and infiltration is known to be dependent on interaction of the leukocytes with the endothelial cell surface via a class of glycoproteins collectively known as endothelial cell adhesion molecules (ECAMs). Several recent studies suggest that NO may modulate cytokine-induced ECAM expression in cultured endothelial cells in vitro by regulating the activation of nuclear transcription factor kappa B (NF-kappaB). This discussion reviews some of the more recent studies that assess the role of the different NOS isoforms on the inflammatory response in vivo.
