To elucidate the possible role of chemical mediators patients with cirrhosis, whose altered host-defense in modulating the host-defense activity of patients with abilities have been well described. [5][6][7][8] We have precirrhosis, primary-cultured human hepatic macroviously investigated the mediator-releasing ability of phages (HHMF) were obtained from cirrhotic and nonprimary-cultured HHMF derived from patients with cirrhotic patients who received liver resections because normal and cirrhotic livers. 12 We found that HHMF of the presence of malignant liver tumors. The cirrhotic derived from cirrhotic patients released less superoxide and noncirrhotic groups consisted of patients with simi-(P รต .01) and slightly more interleukin (IL-1) (P รต .1) lar malignancies: noncirrhotic patients had normal liver than HMF derived from patients with normal livers, function and normal liver histology for nontumorous but prostaglandin-E 2 (PGE 2 ) production was similar portions. The cultured HHMF were analyzed for their in the two groups. In contrast, earlier animal studies ability to release chemical mediators with specific activities in the host defense system. Dose-dependent in-indicated that HMF derived from rats with CCL 4 -increases in superoxide release, interleukin-1 (IL-1) duced cirrhosis released significantly less O 2 0 and release, and, within a relatively narrow range, prosta-PGE 2 (P รต .01), and higher than normal levels of IL-1 glandin-E 2 (PGE 2 ) release were observed in opsonized (P รต .01). [6][7][8] This observed discrepancy may be because zymosan (oz)-stimulated HHMF derived from both cirof the tremendous variation in the backgrounds and rhotic and noncirrhotic patients. The release of O 2 0 and histories of the human patients. In previous studies, PGE 2 from HHMF derived from cirrhotic patients was subjects with both malignant tumors and benign dissignificantly less than HHMF derived from noncirrhotic eases such as hemangiomas and giant cysts were inpatients, whereas the release of IL-1 was significantly cluded, because of the difficulty in obtaining sufficient greater. Although, because of the limited sample availnumbers of human samples and in predicting the effect ability, only tumor-bearing patients were studied, the mediator-releasing ability of HHMF derived from cir-of tumors on the experimental results. Thus, interpretrhotic patients was significantly different from the abiling the data was difficult, because almost all of the ity of HHMF derived from noncirrhotic patients with cirrhotic patients had to undergo liver resection besimilar malignancies. This phenomenon may be related cause of the presence of malignant tumors. Therefore, to altered host defenses in patients with cirrhosis. (HEPin the present study, we analyzed the functional activi-