Macrophage regulation of myelopoiesis is altered by exposure to the benzene metabolite hydroquinone.

Macrophage regulation of myelopoiesis is altered by exposure to the benzene metabolite hydroquinone.
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巨噬细胞对骨髓生成的调节因接触苯代谢物氢醌而改变。

DOI:
10.1016/0041-008x(89)90249-4
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发表时间:
1989
影响因子:
3.8
通讯作者:
Wierda,D
Wierda,D
中科院分区:
医学3区
文献类型:
--
作者:
Thomas,DJ;Reasor,MJ;Wierda,D

文献摘要

被引文献

相似文献

氢醌是苯的一种骨髓毒性代谢物,在体外降低小鼠骨髓基质细胞支持骨髓生成的能力。骨髓基质由巨噬细胞和成纤维样基质细胞组成,它们协同参与调节骨髓生成。这项研究的目的是确定巨噬细胞或成纤维细胞功能对氢醌的骨髓毒性作用更敏感。为了解决这个问题,我们建立了巨噬细胞和成纤维样基质细胞的纯化群体,并用氢醌处理每个群体。这些细胞与未处理的相反类型的细胞一起重组,并检测它们在琼脂覆盖层中支持粒细胞和巨噬细胞克隆形成的能力。含有氢醌处理的巨噬细胞的重组培养物比含有未经处理的巨噬细胞的相应培养物支持的集落更少。含有氢醌处理的成纤维样基质细胞的重组培养物不受影响。此外,对苯二酚降低了脂多糖刺激的纯化巨噬细胞中可检测到的白细胞介素1活性。这些结果表明,氢醌选择性地干扰巨噬细胞的功能,可能部分是通过改变巨噬细胞分泌IL-1来实现的。
Hydroquinone, a myelotoxic metabolite of benzene, decreases the ability of murine bone marrow stromal cells to support myelopoiesis in vitro. Bone marrow stroma consists of macrophages and fibroblastoid stromal cells that participate coordinately in regulating myelopoiesis. The goal of this study was to determine if macrophage or fibroblastoid cell function is more sensitive to the myelotoxic actions of hydroquinone. To address this question, we developed purified populations of macrophages and fibroblastoid stromal cells and treated each population with hydroquinone. These cells were reconstituted together with nontreated cells of the opposite type and assayed for their ability to support the formation of granulocyte and macrophage colonies in an agar overlay. Reconstituted cultures containing hydroquinone-treated macrophages supported fewer colonies than did corresponding cultures containing untreated macrophages. Reconstituted cultures containing hydroquinone-treated fibroblastoid stromal cells were not affected. Moreover, hydroquinone reduced detectable interleukin-1 activity in purified macrophage cultures stimulated with lipopolysaccharide. These results indicate that hydroquinone selectively interferes with macrophage function possibly, in part, via alteration of macrophage interleukin-1 secretion.