Effect of infection by lactic dehydrogenase virus on expression of intercellular adhesion molecule-1 on vascular endothelial cells of pancreatic islets in streptozotocin-induced insulitis of CD-1 mice.

Streptozotocin (SZ)-induced insulitis, which is an animal model for insulin-dependent diabetes mellitus, was suppressed by lactic dehydrogenase virus (LDV) infection. There were no differences in degenerative and necrotic changes of islet cells between SZ-treated mice and SZ-treated mice with LDV infection during the pre-insulitis phase. The degree of insulitis was more severe and the plasma glucose levels were higher in SZ-treated mice than in SZ-treated mice with LDV infection. Severe degenerative and necrotic changes of cells with mononuclear cell infiltration into the islets were seen in the SZ-treated mice. Infiltration of these cells into islets was less in SZ-treated mice with LDV infection. During the pre-insulitis phase, there was slight expression of intercellular adhesion molecule-1 (ICAM-1) on the surface of vascular endothelial cells in and/or around islets in both groups. ICAM-1 expression on vascular endothelial cells increased in parallel to the degree of insulitis. The degree of this expression in SZ-treated mice was higher than in SZ-treated mice with LDV infection. These results suggest that expression of ICAM-1 on vascular endothelial cells in SZ-treated mice may be important for the development of insulitis. Also, decreased expression of ICAM-1 in the islets may be responsible for the inhibition of the development of insulitis seen in SZ-treated mice with LDV infection.