Chronic alcohol consumption is associated with changes in the distribution, immunophenotype, and the inflammatory cytokine secretion profile of circulating dendritic cells

被引:69
作者
Javier Laso, Francisco
Vaquero, Jose Miguel
Almeida, Julia
Marcos, Miguel
Orfao, Alberto
机构
[1] Univ Hosp, Serv Med Interna 2, Unidad Alcoholismo, Salamanca 37007, Spain
[2] Univ Salamanca, Serv Citometria, E-37008 Salamanca, Spain
[3] Univ Salamanca, Ctr Invest Canc, E-37008 Salamanca, Spain
关键词
dendritic cells; alcohol; alcoholism; liver cirrhosis; immune response;
D O I
10.1111/j.1530-0277.2007.00377.x
中图分类号
R194 [卫生标准、卫生检查、医药管理];
学科分类号
摘要
Background: Alcoholism is frequently associated with altered immune responses, limited information being available on its effects on dendritic cells (DC). In the present study we analyze the effects of chronic alcoholism on circulating DC. Methods: For the first time we studied the numerical distribution of DC in peripheral blood (PB), their immunophenotype, and their ex vivo pattern of spontaneous cytokine secretion, in chronic alcoholic patients without liver disease (AWLD group; n=17) and active ethanol (EtOH) intake, as well as in subjects with alcohol liver cirrhosis (ALC group; n=21). Results: A significantly decreased HLADR expression and an increased reactivity for CD123 was observed on PB DC from AWLD patients; additionally, increased secretion of interleukin (IL) 1 beta, IL6, IL12, and tumor necrosis factor-alpha (TNF alpha) by DC was also noted in this group. Conversely, patients with ALC and at least 1 year of alcohol withdrawal (ALCAW group) showed a decreased number of total circulating DC, whereas ALC patients with active EtOH intake (ALCET group) had an abnormally low production of IL1 beta and TNF alpha by PB DC. Conclusion: Chronic alcoholism in the absence of liver disease is associated with an increased secretion of inflammatory cytokines by PB DC, whereas ALCAW and ALCET patients show decreased numbers of circulating DC and reduced secretion of these cytokines, respectively.
引用
收藏
页码:846 / 854
页数:9
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