Chemical mediators released from hepatic macrophages in primary culture--basic characteristics of human hepatic macrophages and changes in liver cirrhosis.

Chemical mediators released from human hepatic macrophages (HHM phi) in primary cultures were analyzed for their secretory function and probable contribution to the modulation of the host defense system and metabolism in liver cirrhosis. In our basic studies, HHM phi increased dose dependently the release of superoxide (O2-) and interleukin-1 (IL-1) when stimulated by opsonized zymosan, up to 1000 micrograms/dish. PGE2 production showed a relatively narrow range of dose dependency, and larger doses led to a reduction of PGE2 yield in some samples. Next, we compared the mediator release from the HHM phi of patients with liver cirrhosis with that from HHM phi in normal liver. O2- released from HHM phi of 8 patients with liver cirrhosis was significantly decreased (controls, n = 20) (P < 0.01). IL-1 released from the HHM phi of 6 cirrhotic patients tended to be higher than that from the HHM phi of 10 control patients, but the difference was not statistically significant (P < 0.10). PGE2 production, however, was about the same in the two groups. These results suggest that cultured HHM phi have certain basic characteristics in releasing mediators with highly potent specific activities and also that these secretory abilities may change in liver cirrhosis. In conclusion, the analysis of cultured HHM phi may be a very practical way to clarify their inherent abilities and participation in the complicated clinical features of liver cirrhosis.