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Interleukin-12-induced adhesion molecule expression in murine liver
K J Myers1, M J Eppihimer, L Hall
1Department of Inflammation and Autoimmune Diseases, Hoffman-La Roche, Inc., Nutley, New Jersey, USA.
The American Journal of Pathology
|February 18, 1998
Summary
Interleukin-12 (IL-12) induces liver inflammation by increasing leukocyte infiltration and up-regulating adhesion molecules like ICAM-1 and VCAM-1 in mice. This impacts potential therapeutic uses, especially in liver or autoimmune diseases.
Area of Science:
- Immunology
- Hepatology
- Molecular Biology
Background:
- Systemic administration of interleukin-12 (IL-12) triggers liver inflammation in mice.
- This inflammation is characterized by Kupffer cell changes, hepatocyte necrosis, and leukocyte accumulation.
Purpose of the Study:
- To investigate the expression of adhesion molecules in the livers of mice treated with IL-12.
- To understand the role of these molecules in IL-12-induced liver inflammation.
Main Methods:
- Immunohistochemical staining was employed to visualize adhesion molecule expression.
- Radiolabeled antibody quantitation was used to measure adhesion molecule levels.
- Analysis focused on livers of mice receiving daily doses of murine IL-12.
Main Results:
- Infiltrating leukocytes expressed LFA-1, VLA-4, MAC-1, and CD18, with minimal L-selectin.
- Kupffer cells showed constitutive LFA-1 and MAC-1 expression.
- IL-12 treatment upregulated ICAM-1 and VCAM-1 expression significantly, with de novo expression observed on bile duct epithelia and endothelial cells.
Conclusions:
- IL-12 treatment markedly increases adhesion molecule expression in the liver.
- These changes in adhesion molecules may influence the therapeutic application of IL-12.
- Particular caution is advised for patients with liver disease or autoimmune conditions due to potentially critical roles of adhesion molecules in pathogenesis.