알콜 급식이 마우스의 IL-2 및 IL-6 生産과 腫瘍發生 그리고 其他 免疫反應 潛在力에 미치는 影響 = Effect of Alcohol Feeding on IL-2 and IL-6 production, and Tumorigenesis and Other Immune Response Potential in Mice

다국어 초록 (Multilingual Abstract)

The present study was undertaken to investigate the effect of ethanol feeding on IL2 and IL6 production, carcinogenesis induced by 3-Methylcholanthrene(MCA), natural killer cell activity(NKCA) and by other parameters of immunocompetency in ICR mice. Mice and rats were fed ad libitum both pellet and 10% ethanol(EOH) solution in their drinking water for various period(44-304 days). Control animals were fed a similardiet and water. It was found that mice fed EOH for 44 or 210 days showed a significant suppression in contact hypersen sitivity to dinitrofluorobenezne(DNFB), delayed -type hypersensitivity to d in it rofluorobenezne(DNFB), delayed-type hypersensitivity(DTH) reaction to sheep red blood cell(SRBC), a thymusOdependent antigen, polyvinylpyrrolidone(PVP), a thymus-independent antigen. The contiuous feeding of EOH for 60or 304 days before C. neoformans infection enhanced significantly the recovery of C. neoformans from brain, lung, liver and spleen of the infected mice as compared with that of control mice and the degree of this enhancement appeared to be greater in mice receiving EOH for longer duration. The mice feed EOH for215 dyas before, during and after gestation demonstrated the greater litter size and higher neonatal mortalityas compared with control, indicating prenatal EOH exposure may greatly affect the fetus. In an experiment designed to investigate the effect of EOH feeding on the production of IL-2 and IL-6 by thymocytes and splenocytes of mice, it was demonstrated that EOH feeding for 131 days did not cause any change in the capability of IL-2 production by their thymocytes and splenocytes. Interestingly, however, EOH feeding for the same duration clearly enhanced the IL-6 production by their thymocytes, but by their splenocytes. Fo rthe evaluation of the effect of EOH on carcinogenesis induced by MCA, the frequency of tumor production, the number of tumors per tumor bearing mouse(TBM) and average diameter of the largest tumor per TBM were examined as a function of time after initial MCA Mice fed EOH for 110 days before initial application of MCA showed higher frequency of tumor production when observed at 45th, 65th and 80th days, but not at 95th day, and also showed greater in both number of tumor per TBM and size of the largest tumor as compared with controls, strongly indicating that EOH may increase the incidence of cancer.
To investigate the possible mechanisms responsible for enhancing effect of carcinogenesis, NKCA of splenocyte of ICR mice and Sprague-Dawley rats against YAC-1 cell was assessed by "single cell level assay". NKCA EOH may be responsible, at least in part, for enhancement of tumor induction and tumor growth, acting as promotor. Taken together, the present study strongly suggests, that EOH feeding may enhance IL-6 production, but not IL-2, and may suppress the NKCA and results in enhancement of the tumor production and tumor growth. This study also suggest that EOH feeding may suppress the humiral and cellular immune response and increase the susceptibility of mice to C.neoformans and that EOH feeding before, during and after pregnancy may affcet litter size and neonatal death.