In vitro and in vivo studies of cellular immunity in alcoholic cirrhosis

Hepatic resection for hepatocellular carcinoma in the elderly

“…Although data about the role of alcohol in the development of HCC are inconsistent, the mechanisms that have been proposed include the induction of tumorigenesis secondary to alcoholic cirrhosis [44], a direct tumor initiating and promoting effect of ethanol through induction of various enzymes [45], alterations of DNA repair [46], dietary deficiencies [47], immunosuppression [48], and depletion of hepatic antitumor factors [49]. Poynard et al [50] reported that alcohol abuse has a stronger association with progression of fibrosis with carcinogenesis than virological factors in patients with HCV infection, but not HBV infection.…”

Soluble interleukin-2 receptor and soluble CD8 in liver cirrhosis and obstructive jaundice

“…Both liver cirrhosis and obstructive jaundice are known to result in some kind of immune defect: liver cirrhosis results in polyclonal hypergammaglobulinaemia with enhanced concentrations of IgG, IgM, IgA (Feizi, 1968;Wilson et al, 1969;Iturriaga et al, 1977;Husby et al, 1977) and IgE (van Epps et al, 1976), but cellular immunity is defective; peripheral blood T cells (Bereny et al, 1974;Thomas et al, 1976), delayed-type hypersensitivity (MacSween & Thomas, 1973;Berenyi et al, 1974;Thomas, 1977), lymphocyte proliferation (MacSween & Thomas, 1973;Berenyi et al, 1974) and natural killer cell function (Nakamura (? ;Charpentiere/fl/., 1984) are all diminished in liver cirrhosis.…”

“…In general, liver diseases such as cirrhosis (Thomas, 1977;Berenyi, Straus & Cruz, 1974;MacSween & Thomas, 1973) and obstructive jaundice (Roughneen et ai, 1986;Feduccia, ScottConner & Grogan, 1988;Vane et ai, 1988) result in depressed immune function. In cirrhosis there is also a polyclonal hypergammaglobuhnaemia (Feizi, 1968;Wilson, Onstad & Williams, 1969;Iturriaga et ai, 1977;Husby et ai, 1977), suggesting overactivation of some parts ofthe immune system.…”

In vitro Effect of Ethanol on Subpopulations of Human Blood Mononuclear Cells

“…This effect of ethanol is most pronounced for those mitogens which prima rily stimulate T lymphocytes. In vivo observations al so indicate that ethanol reduces lymphocyte function, since the mononuclear blood cell reactivity to T-cell mitogens, the delayed hypersensitivity response to an tigens applied cutaneously, and the rate of leukocyte mobilization into traumatized skin are all reduzed in alcoholic patients [Brayton et al, 1970;Berenyi et al, 1974;Lundy el al.,1975;Bjorkholm, 1980], Ethanol in concentrations occurring in moderately intoxicated patients reduces the number of phagocyt izing cells in vitro. Previous in vivo studies have shown that ethanol reduces the mobilization and the phagocytizing capacity of macrophages in the lung, in the peritoneal cavity and in the macrophages lining the vascular sinusoids in experimental animals [Louria, 1963;Ali and Nolan.…”