ABSTRACT
Communication between Kupffer cells and hepatocytes in liver disease may also be responsible for the initiation of fibrosis. It is well known that Kupffer cells and other macrophages release cytokines, and monocyte condition medium (MCM) obtained from patients with liver disease is fibrogenic. Thus, in the cellular communication between Kupffer cells (or other macrophages) with hepatocytes in liver disease, several cytokines appear to mediate different responses, i.e., IL-1 and reactive oxygen intermediates appear to be involved in the depression of cytochrome P-450-mediated drug-metabolizing enzyme activity, whereas another cytokine appears to be involved in the fibrogenic activity. Furthermore, the induction of glycogenolysis in the liver by PAF is mediated by prostaglandin D2 from Kupffer cells, i.e., the primary interaction of PAF is with the Kupffer cells with subsequent release of prostaglandin and its effect on glucose production in parenchymal cells. Another interaction between Kupffer cells and hepatocytes mediated by prostaglandins released from activated Kupffer cells has been reported.
