Chronic ethanol ingestion by mice increases expression of CD80 and CD86 by activated macrophages.

Chronic ethanol ingestion by mice increases expression of CD80 and CD86 by activated macrophages.
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小鼠长期摄入乙醇会增加活化巨噬细胞的 CD80 和 CD86 表达。

DOI:
10.1016/j.alcohol.2004.01.004
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发表时间:
2004
期刊:
Alcohol (Fayetteville, N.Y.)
影响因子:
--
通讯作者:
Cook,RobertT
Cook,RobertT
中科院分区:
--
文献类型:
--
作者:
Zhu,Xiaoyan;Coleman,RuthA;Alber,Carol;Ballas,ZuhairK;Waldschmidt,ThomasJ;Ray,NancyB;Krieg,ArthurM;Cook,RobertT

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Results from previous studies from our laboratory have shown that T cells obtained from the spleens of C57BL/6 mice that consumed ethanol chronically have increased expression of activation markers and increased second signal–independent production of interferon-gamma (IFN-γ). We now report that in vitro–activated CD11b+splenocytes obtained from C57BL/6 and BALB/c mice that consumed ethanol chronically express increased levels of the T cell co-stimulatory molecules CD80 and CD86. CD11b+splenocytes encompass at least two populations: the CD11b+Gr.1−population, which is primarily monocytes–macrophages, and a smaller CD11b+Gr.1+population, which is in the myelocytic–monocytic cell series and contains precursors of both macrophages and neutrophils. Evaluation of cultures of purified CD11b+cells, obtained from mice that consumed ethanol chronically, incubated overnight, showed increased up-regulation of CD80 and CD86 expression on Gr.1−mouse splenic macrophages. Results of functional studies of purified CD11b+cells have demonstrated that CD11b+cells obtained from C57BL/6 mice that were exposed to ethanol chronically secrete higher levels, in comparison with the levels secreted by CD11b+cells obtained from control animals, of nitric oxide and several proinflammatory cytokines after stimulation by the oligodeoxynucleotide (ODN) CpG 1826. These findings indicate that CD11b+splenocytes are in some way sensitized to activating stimuli by chronic ethanol exposure in vivo. Such cells may contribute to systemic immunodysregulation, including T-cell activation, by providing abnormal second signals to T cells, or through excessive release of cytokines, such as interleukin (IL)-6 or IL-12.
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