Acquired increase in leucocyte binding by intestinal microvascular endothelium in inflammatory bowel disease

被引:89
作者
Binion, DG [1 ]
West, GA
Volk, EE
Drazba, JA
Ziats, NP
Petras, RE
Fiocchi, C
机构
[1] Med Coll Wisconsin, Froedtert Mem Lutheran Hosp, Div Gastroenterol & Hepatol, Milwaukee, WI 53226 USA
[2] Med Coll Wisconsin, Childrens Hosp Wisconsin, Milwaukee, WI 53226 USA
[3] Med Coll Wisconsin, Milwaukee, WI 53226 USA
[4] Case Western Reserve Univ, Univ Hosp Cleveland, Sch Med, Dept Med, Cleveland, OH 44106 USA
[5] Case Western Reserve Univ, Univ Hosp Cleveland, Sch Med, Inst Pathol, Cleveland, OH 44106 USA
[6] Cleveland Clin Fdn, Dept Anat Pathol, Cleveland, OH 44195 USA
[7] Cleveland Clin Fdn, Inst Res, Cleveland, OH 44195 USA
关键词
D O I
10.1016/S0140-6736(98)05050-8
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background Endothelial cells that line microvascular blood vessels have 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 colitis-the two forms of inflammatory bowel disease-display an increased leucocyte-binding capacity in vitro. We investigated whether this enhanced leucocyte binding is a primary or an acquired defect. Methods We cultured human intestinal microvascular endothelial cells (HIMEC) from the uninvolved intestine and chronically inflamed bower of three patients with inflammatory bower disease (two Crohn's disease, one ulcerative colitis). We assessed HIMEC binding to polymorphonuclear leucocytes and U937 cells by means of an adhesion assay. Findings After activation with interleukin-la or lipopolysaccharide, HIMEC from the chronically inflamed tissue in all three patients with inflammatory bowel disease bound as many polymorphonuclear cells as endothelial cells from twice U937 leucocytes and uninvolved tissue. Interpretation Enhanced leucocyte 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 key regulatory step in the inflammatory process, this enhanced binding may contribute to the pathophysiology of chronic intestinal inflammation.
引用
收藏
页码:1742 / 1746
页数:5
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