ACQUIRED INCREASE IN LEUKOCYTE BINDING BY INTESTINAL MICROVASCULAR ENDOTHELIUM IN INFLAMMATORY BOWEL-DISEASE

Citation
Dg. Binion et al., ACQUIRED INCREASE IN LEUKOCYTE BINDING BY INTESTINAL MICROVASCULAR ENDOTHELIUM IN INFLAMMATORY BOWEL-DISEASE, Lancet, 352(9142), 1998, pp. 1742-1746
Citations number
26
Categorie Soggetti
Medicine, General & Internal
Journal title
LancetACNP
ISSN journal
01406736
Volume
352
Issue
9142
Year of publication
1998
Pages
1742 - 1746
Database
ISI
SICI code
0140-6736(1998)352:9142<1742:AIILBB>2.0.ZU;2-Z
Abstract
Background Endothelial cells that line microvascular blood vessels hav e an important role in inflammation through their ability to bind and recruit circulating leucocytes. Endothelial cells from the intestines of patients with chronically inflamed Crohn's disease and ulcerative c olitis-the two forms of inflammatory bowel disease-display an increase d leucocyte-binding capacity in vitro. We investigated whether this en hanced leucocyte binding is a primary or an acquired defect. Methods W e cultured human intestinal microvascular endothelial cells (HIMEC) fr om the uninvolved intestine and chronically inflamed bower of three pa tients with inflammatory bower disease (two Crohn's disease, one ulcer ative colitis). We assessed HIMEC binding to polymorphonuclear leucocy tes and U937 cells by means of an adhesion assay. Findings After activ ation with interleukin-la or lipopolysaccharide, HIMEC from the chroni cally inflamed tissue in all three patients with inflammatory bowel di sease bound as many polymorphonuclear cells as endothelial cells from twice U937 leucocytes and uninvolved tissue. Interpretation Enhanced l eucocyte binding by HIMEC from chronically inflamed tissue in patients with inflammatory bowel disease is an acquired defect since it is not found in the uninvolved intestinal segments from the same individuals . Because interaction between endothelial cells and leucocytes is a ke y regulatory step in the inflammatory process, this enhanced binding m ay contribute to the pathophysiology of chronic intestinal inflammatio n.