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Chemical mediators released by primary‐cultured human hepatic macrophages in patients with and without cirrhosis: A study in tumor‐bearing patients
Author(s) -
Funaki N,
Arii S,
Monden K,
Higashitsuji H,
Furutani M,
Mise M,
Tanaka J,
Imamura M
Publication year - 1996
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.510230610
Subject(s) - cirrhosis , primary (astronomy) , bearing (navigation) , medicine , gastroenterology , chemistry , cancer research , immunology , physics , cartography , astronomy , geography
To elucidate the possible role of chemical mediators in modulating the host‐defense activity of patients with cirrhosis, primary‐cultured human hepatic macrophages (HHMΦ) were obtained from cirrhotic and noncirrhotic patients who received liver resections because of the presence of malignant liver tumors. The cirrhotic and noncirrhotic groups consisted of patients with similar malignancies: noncirrhotic patients had normal liver function and normal liver histology for nontumorous portions. The cultured HHMΦ were analyzed for their ability to release chemical mediators with specific activities in the host defense system. Dose‐dependent increases in superoxide release, interleukin‐1 (IL‐1) release, and, within a relatively narrow range, prostaglandin‐E 2 (PGE 2 ) release were observed in opsonized zymosan (oz)‐stimulated HHMΦ derived from both cirrhotic and noncirrhotic patients. The release of O 2 ‐ and PGE 2 from HHMΦ derived from cirrhotic patients was significantly less than HHMΦ derived from noncirrhotic patients, whereas the release of IL‐1 was significantly greater. Although, because of the limited sample availability, only tumor‐bearing patients were studied, the mediator‐releasing ability of HHMΦ derived from cirrhotic patients was significantly different from the ability of HHMΦ derived from noncirrhotic patients with similar malignancies. This phenomenon may be related to altered host defenses in patients with cirrhosis.