Ethanol as a possible cofactor in the development of murine AIDS.
Ethanol as a possible cofactor in the development of murine AIDS.
复制标题
乙醇作为小鼠艾滋病发展的可能辅助因子。
DOI：
10.1111/j.1530-0277.1995.tb00967.x
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Cohen,DA
中科院分区：
文献类型：
--
作者：
Fitzpatrick,EA;Rhoads,CA;Espandiari,P;Kaplan,AM;Cohen,DA
Chronic ethanol (EtOH) abuse in humans leads to a variety of immuno‐modulatory events that can alter resistance to a number of infectious agents. Whether alcohol abuse affects the susceptibility to human immunodeficiency virus infection or the subsequent development of acquired immune deficiency syndrome (AIDS) is a matter of extreme importance; however, available information in humans or animal models is limited. The goal of this study was to evaluate the effect of chronic EtOH feeding in mice on the development of immunodeficiency in the murine model of AIDS (MAIDS). C57BV6 mice were placed on the Lieber‐DeCarli liquid EtOH diet pS% or 31% total caloric intake) or a nutrient‐matched isocaloric Quid control diet. Seven days later, mice were infected with the LP‐BMS murine leukemia virus mixture, and groups of infected and noninfected mice were assayed at defined time points postinfection for antigen‐specific and nonspecific immune responses. In the absence of retroviral infection, chronic EtOH feeding (5–8 weeks) led to reductions in spleen weights, compared with isocaloric controls. In spite of reduced spleen size, mitogenic responses of spleen cells to concanavalin A (ConA) and lipopolysaccharide (LPS) were elevated in EtOH‐fed mice, as compared with mice fed the control diet. Chronic EtOH feeding also enhanced the allogeneic mixed lymphocyte response and increased antigen‐specific priming of both B‐cells and CD4+T‐cells to the antigen, sheep red blood cells. In MAIDS‐infected mice, chronic EtOH feeding delayed but did not prevent the onset of virus‐induced immunodeficiency and MAIDS‐induced autoantibody synthesis. In contrast to mice with MAIDS infection alone, infected mice fed an EtOH diet displayed significant mitogenic responses to ConA and LPS at 4 weeks postinfection; however, at 8 weeks postinfection, both groups were completely immunosuppressed. Liver damage was detected in all groups of EtOH‐fed mice, as indicated by the elevated liver enzymes, ALT and‘ASR moreover, MAIDS infection did not alter the extent of liver damage caused by EtOH feeding. These data suggest that chronic feeding of the Lieber‐DeCarli EtOH diet in mice can lead to immune enhancement and that under these conditions causes a delay in the onset of MAIDS. Whether these results are caused by the effects of chronic exposure of the immune system to EtOH or to elevated Went levels in the standard Lieber‐DeCarli liquid EtOH diet is discussed.
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在导致小鼠艾滋病的逆转录病毒感染过程中，吗啡和乙醇治疗导致淋巴细胞和巨噬细胞亚群发生变化。
影响因子：
6.1
作者：
Ronald R. Watson;Rao H. Prabhala;H. Darban;M. D. Yahya;Tom L. Smith;Tom L. Smith
通讯作者：
Tom L. Smith
乙醇诱导的小鼠细胞介导的免疫抑制。
DOI：
10.1111/j.1530-0277.1992.tb01386.x
发表时间：
1992
期刊：
Alcoholism, clinical and experimental research
影响因子：
--
作者：
Ruani Jayasinghe;Gerald Gianutsos;Andrea K. Hubbard
通讯作者：
Andrea K. Hubbard
影响因子：
4.4
作者：
D. Klinman;H. Morse
通讯作者：
D. Klinman;H. Morse
酒精性肝病的免疫学方面。
影响因子：
29.4
作者：
R. Zetterman;R. Zetterman;Michael F. Sorrell;Michael F. Sorrell
通讯作者：
Michael F. Sorrell
通过施用抗DNA的抗独特型抗体来抑制小鼠狼疮性肾炎。
DOI：
--
发表时间：
1984
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Hahn,BH;Ebling,FM
通讯作者：
Ebling,FM