title: Differential expression of cell adhesion molecules within inflamed ileal pouch mucosa: relationship to recruited cell subtypes.
abstract: BACKGROUND
  Endothelial-bound cell adhesion molecules are important in recruiting inflammatory cells to the mucosa in inflammatory bowel disease (IBD). Little is known of the expression of these molecules in relation to the recruitment of particular cell subtypes in the early course of mucosal inflammation. We therefore studied the expression of several adhesion molecules to examine their potential correlation with the cellular infiltrate in the inflamed ileal pouch, a possible disease model for ulcerative colitis.
  
  
  METHODS
  Eleven patients (group 1) with familial adenomatous polyposis (FAP) with no evidence of ileal pouch inflammation and 14 patients (group 2) with ileal pouch inflammation (all with a prior diagnosis of ulcerative colitis) underwent pouch endoscopy with biopsy. Cryostat sections of biopsies were immunostained using a three-stage immunoperoxidase method for the adhesion molecules intercellular adhesion molecule (ICAM-1), vascular cellular adhesion molecule (VCAM-1), E-selectin and mucosal addressin cell adhesion molecule 1 (MAdCAM-1). These results were correlated with immunostaining for the cell markers CD3, CD4, CD8, CD45RO, CD14 and CD15, which were quantified by computer image analysis.
  
  
  RESULTS
  MAdCAM-1, ICAM-1 and VCAM-1 were expressed to similar degrees on the endothelia of groups 1 and 2. In contrast, E-selectin was significantly increased in group 2 (P = 0.003) and correlated with immunostaining for CD15 (r = 0.72), CD4 (r = 0.55) and CD14 (r = 0.53). MAdCAM-1 expression did not correlate with any cell subset. CD15 was the only cell marker to be altered significantly, being increased in group 2 (P = 0.002).
  
  
  CONCLUSIONS
  The inflammatory process seen in ileal pouch inflammation is characterized by up-regulation of E-selectin and recruitment of CD15-positive cells, emphasizing the role of neutrophil recruitment and migration to the epithelium in the pathogenesis of this condition.
authors: Department of Gastroenterology, St Mark's Hospital, Harrow, UK.
authors: P D
authors: PD
authors: Thomas
authors: A
authors: A
authors: Forbes
authors: A B
authors: AB
authors: Price
authors: R J
authors: RJ
authors: Nicholls
authors: P J
authors: PJ
authors: Ciclitira
mesh_terms: D011125:Adenomatous Polyposis Coli / Q000378:metabolism*; D000328:Adult; D000368:Aged; D015815:Cell Adhesion Molecules; D002465:Cell Movement; D019040:E-Selectin / Q000378:metabolism; D005260:Female; D006801:Humans; D007124:Immunoenzyme Techniques; D007136:Immunoglobulins / Q000032:analysis*; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism*; D007413:Intestinal Mucosa; D016256:Lewis X Antigen; D008297:Male; D008875:Middle Aged; D009088:Mucoproteins / Q000032:analysis*; D020556:Neutrophil Infiltration; D016201:Receptors, Lymphocyte Homing / Q000378:metabolism*; D015854:Up-Regulation; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism*
chemical_list: D015815:Cell Adhesion Molecules; D019040:E-Selectin; D007136:Immunoglobulins; D016256:Lewis X Antigen; C504265:MADCAM1 protein, human; D009088:Mucoproteins; D016201:Receptors, Lymphocyte Homing; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1