Abstract
When the heat-killed Propionibacterium acnes (P. acnes) was injected into mouse through tail vein, macrophages including Kupffer cells accumulate in the liver reaching its maximum 7 days later. To study the function of these liver adherent cells, production of tumor necrosis factor (TNF) and its regulation by prostaglandins (PGs) were investigated in BALB/c mouse and C3H/HeJ mouse. As a result, in BALB/c mouse, P. acnes-elicited liver adherent cells and Kupffer cells produced TNF by stimulating with endotoxin lipopolysaccharide in dose-dependent manner, but in C3H/HeJ mouse, not. When, in BALB/c mouse, these liver adherent cells and Kupffer cells were treated with PGE and PGI2, production of TNF was significantlly reduced. These results suggested that TNF may play a role in the induction of acute hepatic cell necrosis model, and inhibition of TNF production by liver adherent cells and Kupffer cells possibly suppress liver injury in this model.
