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Updated: Oct 19, 2026

Dynamic Adhesion Assay for the Functional Analysis of Anti-adhesion Therapies in Inflammatory Bowel Disease
Published on: September 20, 2018
In situ expression of E-selectin and intercellular adhesion molecule-1 in chronic inflammatory diseases of the
A C Lazaris1, C Dicoglou, S Tseleni-Balafouta
1Department of Pathology, Athens National University Medical School, Greece.
Aim:
The study of cell adhesion molecules contributes to our understanding of the inflammatory mechanisms which include the endothelial activation of newly formed or pre-existing vessels, the increase of inflammatory cells' adhesive capability and their migration into perivascular tissues. The aim of the present study was to investigate the local presence and the extent of expression of E-selectin and intercellular adhesion molecule-1 (ICAM-1) in the mucosa of patients with chronic gastritis, chronic inflammatory bowel disease, and controls, as well as to identify possible correlations between in situ expression of the above adhesion molecules and degree of inflammatory activity or therapeutic response.
Design:
In cryostat tissue sections we examined the immunohistochemical expression and localization of E-selectin and the intercellular adhesion molecule-1 (ICAM-1). Our specimens consisted of 27 cases of chronic gastritis, 42 cases of ulcerative colitis, and 15 cases of Crohn's disease.
Results:
E-selectin was expressed in capillary endothelia as well as on neutrophils, located either in the lamina propria or in the glandular epithelia or lumina. This marker's expression was associated with the active phase of ulcerative colitis (p<0.0005) and possibly of chronic gastritis (p=0.06). ICAM-1 immunolabelling was localized in endothelia and chronic inflammatory components which had passed through the vascular walls. This marker's immunoreactivity was generally increased in all our specimens compared to normal mucosa and generally tended to correlate with chronic phases of the inflammatory process (p<0.10).
Conclusions:
E-selectin regulates the accumulation of neutrophils in the early stages of the inflammatory process and is thus associated at least with the active phase of ulcerative colitis. Whether any post-therapy alteration of E-selectin immunopositivity seems to indicate a good response to drug therapy is well worth investigating in ulcerative colitis patients. ICAM-1 immunoreactivity in lymphoplasmacytic infiltrates might serve as a marker of chronic immune stimulation, which is potentially responsible for the persistence of the inflammatory disorders.
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