Detection of ICAM-1 in experimentally induced colitis of ICAM-1-deficient and wild-type mice: An immunohistochemical study

Citation
F. Bendjelloul et al., Detection of ICAM-1 in experimentally induced colitis of ICAM-1-deficient and wild-type mice: An immunohistochemical study, HISTOCHEM J, 32(12), 2000, pp. 703-709
Citations number
60
Categorie Soggetti
Medical Research Diagnosis & Treatment
Journal title
HISTOCHEMICAL JOURNAL
ISSN journal
00182214 → ACNP
Volume
32
Issue
12
Year of publication
2000
Pages
703 - 709
Database
ISI
SICI code
0018-2214(200012)32:12<703:DOIIEI>2.0.ZU;2-W
Abstract
Adhesion molecules (e.g. ICAM-1, CD 54) are known to be upregulated on acti vated vascular endothelial cells during inflammatory reactions. To study th e role of ICAM-1 in intestinal inflammation in vivo, we induced acute exper imental colitis in wild-type (C57BL/6) mice and ICAM-1-deficient mice, by f eeding the animals with 3% dextran sodium sulphate (DSS) in drinking water for 7 days. In the control strain the immunohistochemical staining showed a very pronounced endothelial upregulation of ICAM-1 after the DSS treatment observed in areas of inflammatory infiltrate, especially in venules or art erioles of the propria and submucosa, and partly in the mesocolon. DSS-fed ICAM-1-deficient mice showed no endothelial enhancement and only faint stai ning of venules or capillaries approaching that encountered in the control ICAM-1-deficient animals. Our data indicate that ICAM-1 may play a crucial role in the development of acute intestinal inflammation, consistent with o ur finding that ICAM-1 deficiency can obviate severe forms of experimentall y induced colitis in mice.