title: Acquired increase in leucocyte binding by intestinal microvascular endothelium in inflammatory bowel disease.
abstract: 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 bowel of three patients with inflammatory bowel disease (two Crohn's disease, one ulcerative colitis). We assessed HIMEC binding to polymorphonuclear leucocytes and U937 cells by means of an adhesion assay.
  
  
  RESULTS
  After activation with interleukin-1beta or lipopolysaccharide, HIMEC from the chronically inflamed tissue in all three patients with inflammatory bowel disease bound twice as many polymorphonuclear leucocytes and U937 cells as endothelial cells from uninvolved tissue.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Division of Gastroenterology and Hepatology, Froedtert Memorial Lutheran Hospital, Children's Hospital of Wisconsin and Medical College of Wisconsin, Milwaukee 53226, USA. dbinion@mcw.edu
authors.forename: D G
authors.initials: DG
authors.lastname: Binion
authors.forename: G A
authors.initials: GA
authors.lastname: West
authors.forename: E E
authors.initials: EE
authors.lastname: Volk
authors.forename: J A
authors.initials: JA
authors.lastname: Drazba
authors.forename: N P
authors.initials: NP
authors.lastname: Ziats
authors.forename: R E
authors.initials: RE
authors.lastname: Petras
authors.forename: C
authors.initials: C
authors.lastname: Fiocchi
mesh_terms: D000328:Adult; D015815:Cell Adhesion Molecules / Q000032:analysis; D002478:Cells, Cultured; D003093:Colitis, Ulcerative / Q000276:immunology* / Q000473:pathology; D003424:Crohn Disease / Q000276:immunology* / Q000473:pathology; D004730:Endothelium, Vascular / Q000276:immunology* / Q000473:pathology; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D007413:Intestinal Mucosa / Q000098:blood supply / Q000276:immunology / Q000473:pathology; D007957:Leukocyte Adherence Inhibition Test; D007962:Leukocytes / Q000276:immunology* / Q000473:pathology; D008297:Male; D008833:Microcirculation / Q000276:immunology / Q000473:pathology; D009504:Neutrophils / Q000276:immunology / Q000473:pathology; D016028:Receptors, Leukocyte-Adhesion / Q000276:immunology*
chemical_list: D015815:Cell Adhesion Molecules; D016028:Receptors, Leukocyte-Adhesion