Intercellular adhesion molecules (ICAMs) are molecules that promote adhesion between cells. Examples include adhesion from most white blood cells, related to their immunological response to wound or bacterial infection.
During the acute stages of inflammation, homeostasis is altered, resulting in the cytokine stimulated release of ICAMs which promote leukocyte adherence to the endothelium. The CAMs are involved with leukocyte adhesion at relatively low shear forces and they cause a stronger attachment than selectin molecules.
There are several different forms of ICAM. ICAM-1 is continuously present in low concentrations in the membranes of leukocytes and endothelial cells. Upon cytokine stimulation, the concentrations greatly increase. ICAM-1 can be induced by Interleukin-1 (IL-1) and Tumor Necrosis Factor (TNF) alpha and is expressed by the vascular endothelium, macrophages and lymphocytes.
Adhesion antagonist by herbal medicines
- Crude ethanolic extract of the anti-rheumatic herbal drug gravel root (rhizome of Eupatorium purpureum), was identified as a potent inhibitor of ICAM-1 and some beta 1 and beta 2 integrin-mediated cell adhesions. “It appears that it has therapeutic potential for diseases where integrin adhesion molecules play a significant role.” (Planta Med 1998 Dec;64(8):683-5)The active principle of gravel root has now been isolated and identified as Cistifolin (5-acetyl-6-hydroxy-2,3-dihydro-cis-2-isopropenyl-3- tiglinoyloxybenzofuran). Cistofolin appears to alter T cell production of the macrophage-attracting chemokines CCL3 and CCL4 which appear to alter expression of ICAM-1. cistifolin inhibits the Mac-1 (CD11b/CD18)-dependent monocyte adhesion to fibrinogen in a concentration-dependent manner
- Feverfew (parthenolide) also inhibits the expression of intercellular adhesion molecule-1 (ICAM-1) induced by the cytokines IL-1 and other integrin-mediated leucocyte adhesions.
- Dan shen (Salvia miltiorrhiza down regulates ICAM in liver caaner and metastasis.