CHEMICAL MEDIATORS RELEASED BY PRIMARY-CULTURED HUMAN HEPATIC MACROPHAGES IN PATIENTS WITH AND WITHOUT CIRRHOSIS - A STUDY IN TUMOR-BEARINGPATIENTS

Citation
N. Funaki et al., CHEMICAL MEDIATORS RELEASED BY PRIMARY-CULTURED HUMAN HEPATIC MACROPHAGES IN PATIENTS WITH AND WITHOUT CIRRHOSIS - A STUDY IN TUMOR-BEARINGPATIENTS, Hepatology, 23(6), 1996, pp. 1353-1358
Citations number
23
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
02709139
Volume
23
Issue
6
Year of publication
1996
Pages
1353 - 1358
Database
ISI
SICI code
0270-9139(1996)23:6<1353:CMRBPH>2.0.ZU;2-J
Abstract
To elucidate the possible role of chemical mediators in modulating the host-defense activity of patients with cirrhosis, primary-cultured hu man hepatic macrophages (HHM Phi) were obtained from cirrhotic and non cirrhotic patients who received liver resections because of the presen ce of malignant liver tumors. The cirrhotic and noncirrhotic groups co nsisted of patients with similar malignancies: noncirrhotic patients h ad normal liver function and normal liver histology for nontumorous po rtions. The cultured HHM Phi were analyzed for their ability to releas e chemical mediators with specific activities in the host defense syst em. Dose-dependent increases in superoxide release, interleukin-l (IL- 1) release, and, within a relatively narrow range, prostaglandin-E(2) (PGE(2)) release were observed in opsonized zymosan (oz)-stimulated HH M Phi derived from both cirrhotic and noncirrhotic patients, The relea se of O-2(-) and PGE(2) from HHM Phi derived from cirrhotic patients w as significantly less than HHM Phi derived from noncirrhotic patients, whereas the release of IL-1 was significantly greater. Although, beca use of the limited sample availability, only tumor-bearing patients we re studied, the mediator-releasing ability of HHM Phi derived from cir rhotic patients was significantly different from the ability of HHM Ph i derived from noncirrhotic patients with similar malignancies. This p henomenon may be related to altered host defenses in patients with cir rhosis.