ArticleClinical and experimental immunology1993
Altered expression of cell adhesion molecules in uninvolved gut in inflammatory bowel disease.
Article in Clinical and experimental immunology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 66 citations in OpenAlex.
- Increased Cell Adhesion Molecules, PECAM-1, ICAM-3, or VCAM-1, Predict Increased Risk for Flare in Patients With Quiescent Inflammatory Bowel Disease.Journal of clinical gastroenterology · 2017Article
- Epithelial cell extrusion: Pathways and pathologies.Seminars in cell & developmental biology · 2017Review
- Inflammatory bowel disease and thromboembolism.World journal of gastroenterology · 2014Review
- Adhesion molecules in chronic ulcerative colitis.International journal of colorectal disease · 2007Article
- Soluble selectins, sICAM, sVCAM, and angiogenic proteins in different activity groups of patients with inflammatory bowel disease.Digestive diseases and sciences · 2004Article
- Expression of ICAM-1 in colon epithelial cells: an ultrastructural study performed on in vivo and in vitro models.Virchows Archiv : an international journal of pathology · 2003Article
- Increase in podoplanin-expressing intestinal lymphatic vessels in inflammatory bowel disease.Virchows Archiv : an international journal of pathology · 2003Article
- Article
- Quantification of mucosal leucocyte endothelial cell interaction by in vivo fluorescence microscopy in experimental colitis in mice.Clinical and experimental immunology · 2001Article
- Detection of ICAM-1 in experimentally induced colitis of ICAM-1-deficient and wild-type mice: an immunohistochemical study.The Histochemical journal · 2000Article
- Changed colonic profile of P-selectin, platelet-endothelial cell adhesion molecule-1 (PECAM-1), intercellular adhesion molecule-1 (ICAM-1), ICAM-2, and ICAM-3 in inflammatory bowel disease.Clinical and experimental immunology · 2000Article
- Nuclear factor-kappa B activity and intestinal inflammation in dextran sulphate sodium (DSS)-induced colitis in mice is suppressed by gliotoxin.Clinical and experimental immunology · 2000Article
- Keratinocyte growth factor in inflammatory bowel disease. Increased mRNA transcripts in ulcerative colitis compared with Crohn's disease in biopsies and isolated mucosal myofibroblasts.The American journal of pathology · 1997Article
- Article
- Small bowel transplantation in children: an immunohistochemical study of intestinal grafts.Gut · 1995Article
- Increased expression of cell adhesion molecule P-selectin in active inflammatory bowel disease.Gut · 1995Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adhesion of circulating cells to vascular endothelium occurs in the early phase of inflammation, and is mediated by specific cell adhesion molecules. Many such adhesion molecules are increased in inflamed regions of ulcerative colitis (UC) and Crohn's disease (CD) but there is limited knowledge of their expression in the uninvolved gut, adjacent to inflammation. We investigated immunohistochemically the expression of platelet endothelial cell adhesion molecule-1 (PECAM-1), intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1) on resected specimens taken at a distance of 2-4 cm from the inflamed area and without histological signs of inflammation. Compared with normal gut, we found (i) a significant increase of PECAM-1-positive vessels in the mucosa of uninvolved UC (149.0 +/- 24.1 vessels/mm2 (mean +/- s.d.); normal colon = 123.1 +/- 21.6; P = 0.004); (ii) a significant decrease of ICAM-1-positive vessels in uninvolved CD (111.9 +/- 22.6 vessels/mm2; normal ileum = 136.9 +/- 27.6; P = 0.04); and (iii) a moderate but statistically insignificant increase of LFA-1-positive cells in the mucosa of uninvolved UC and Crohn's ileitis. This altered expression of cell adhesion molecules may contribute to the early lesion in inflammatory bowel disease and provide new therapeutic opportunities.
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