INFLUENCE OF CHRONIC DIETARY ETHANOL ON CYTOKINE PRODUCTION BY MURINESPLENOCYTES AND THYMOCYTES

Citation
Yj. Wang et al., INFLUENCE OF CHRONIC DIETARY ETHANOL ON CYTOKINE PRODUCTION BY MURINESPLENOCYTES AND THYMOCYTES, Alcoholism, clinical and experimental research, 18(1), 1994, pp. 64-70
Citations number
63
Categorie Soggetti
Substance Abuse
ISSN journal
01456008
Volume
18
Issue
1
Year of publication
1994
Pages
64 - 70
Database
ISI
SICI code
0145-6008(1994)18:1<64:IOCDEO>2.0.ZU;2-S
Abstract
Prolonged consumption of ethanol (ETOH) results in alterations of host defense via immune modulation, increasing susceptibility to infection . In the present study, effects of chronic dietary ETOH on cytokine pr oduction by splenocytes and thymocytes, splenocyte and thymocyte proli feration induced by mitogens, splenic natural killer cell activity, an d antibody production (IgA and IgG) were examined. C57BL/6 mice were f ed 5% ETOH v/v in the Lieber-DeCarli liquid diet for 11 weeks. Release of interleukin (IL)-2, IL-5, IL-6, IL-10, and interferon (IFN)gamma p roduced by concanavalin A (Con A) stimulated splenocytes was significa ntly decreased, whereas secretion of IL-4 was slightly decreased by ch ronic dietary ETCH compared with controls. Production of tumor necrosi s factor-alpha and IL-6 by lipopolysaccharide-stimulated splenocytes w as significantly and slightly decreased by ETOH compared with controls , respectively. Splenocyte and thymocyte proliferation induced by Con A was significantly inhibited by ETCH, whereas splenocyte proliferatio n induced by lipopolysaccharide was not affected. Natural killer cell activity was significantly inhibited by ETOH compared with controls. T he production of IgA and IgG by splenocytes were also significantly de creased by ETCH compared with controls. The levels of IL-2, IL-4, and IL-6 produced by Con A-stimulated thymocytes were significantly reduce d by dietary ETOH compared with control, whereas production of IFN-gam ma by thymocytes was not affected. Our results suggest that chronic di etary ETOH alters the cytokine release, thereby impairing immune respo nse and T-cell maturation, which increase host susceptibility to infec tion.