ArticleClinical and experimental immunology2000
Intercellular adhesion molecule-1 (ICAM-1) deficiency protects mice against severe forms of experimentally induced colitis.
Article in Clinical and experimental immunology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 80 citations in OpenAlex.
- Pentoxifylline in patients with ulcerative colitis treated with mesalamine by modulation of IL-6/STAT3, ZO-1, and S1P pathways: a randomized controlled double-blinded study.Inflammopharmacology · 2024Trial
- Anti-inflammatory effects of trans-cinnamic acid through modulation of endothelial ICAM-1 expression and neutrophil recruitment.Journal of natural medicines · 2026Article
- Potential of using an engineered indole lactic acid producing Escherichia coli Nissle 1917 in a murine model of colitis.Scientific reports · 2024Article
- Review
- Modulation of Orosomucoid-like Protein 3 Activity in the Management of Inflammatory Bowel Disease.Journal of biotechnology and biomedicine · 2024Article
- TRPV1 controls innate immunity during Citrobacter rodentium enteric infection.PLoS pathogens · 2023Article
- An Activation-Specific Anti-Mac-1 Designed-Ankyrin-Repeat-Protein Attenuates Colitis in Mice.Life (Basel, Switzerland) · 2023Article
- Review
- Identifying hub genes and miRNAs in Crohn's disease by bioinformatics analysis.Frontiers in genetics · 2022Article
- Phosphatidylserine externalized on the colonic capillaries as a novel pharmacological target for IBD therapy.Signal transduction and targeted therapy · 2021Article
- Vedolizumab: Potential Mechanisms of Action for Reducing Pathological Inflammation in Inflammatory Bowel Diseases.Frontiers in cell and developmental biology · 2021Review
- Assessment of ICAM-1 N-glycoforms in mouse and human models of endothelial dysfunction.PloS one · 2020Article
- ICAM-1 controls development and function of ILC2.The Journal of experimental medicine · 2018Article
- New Data on Human Macrophages Polarization byFrontiers in immunology · 2017Article
- The Dual Role of Neutrophils in Inflammatory Bowel Diseases.Journal of clinical medicine · 2016Review
- Targeting leukocyte trafficking for the treatment of inflammatory bowel disease.Clinical pharmacology and therapeutics · 2015Review
- Positive role of CCAAT/enhancer-binding protein homologous protein, a transcription factor involved in the endoplasmic reticulum stress response in the development of colitis.The American journal of pathology · 2009Article
- Leukocyte adhesion molecules in animal models of inflammatory bowel disease.Inflammatory bowel diseases · 2008Review
- Article
- Oral administration of probiotic bacteria (E. coli Nissle, E. coli O83, Lactobacillus casei) influences the severity of dextran sodium sulfate-induced colitis in BALB/c mice.Folia microbiologica · 2006Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ICAM-1 (CD54), the ligand for LFA-1 and Mac-1, is up-regulated during inflammatory reaction on the activated vascular endothelium. To determine its role in intestinal inflammation, we induced acute experimental colitis in mice with a deleted ICAM-1 gene, by feeding them with 3% dextran sodium sulphate (DSS) in drinking water for 7 days. Chronic colitis was elicited by DSS similarly, followed by 2 weeks with water. In the acute phase of inflammation, ICAM-1-deficient mice exhibited a significantly lower mortality rate (5%) than control C57Bl/6J mice (35%). Control animals, but not the ICAM-1-deficient mice, exhibited diarrhoea and rectal bleeding. Histological examination of large-bowel samples evaluated the intensity of inflammatory changes, and type and extent of mucosal lesions. In the acute phase, 33.3% of samples from ICAM-1-deficient mice exhibited mucosal defects (flat and fissural ulcers), predominantly mild to moderate inflammatory infiltrate within the lamina propria mucosae and lower grades of mucosal lesions. Much stronger inflammatory changes were present in control animals, flat ulcers (sometimes multiple) and fissural ulcers being observed in 62.5% of samples. Mucosal inflammatory infiltrate was moderate to severe, typically with higher grades of mucosal lesions. In chronic colitis, smaller inflammatory changes were found in the large bowel. The two mouse strains differed, the chronic colitis being accompanied by an increased serum level of anti-epithelial IgA autoantibodies in C57Bl/6 control mice but not in ICAM-1-deficient mice. These findings provide direct evidence of the participation of ICAM-1 molecule in the development of experimentally induced intestinal inflammation.
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