Schuschke D A, Saari J T, Miller F N
Department of Physiology and Biophysics, Health Sciences Center A1115, University of Louisville, Louisville, KY 40292, USA.
Immunol Lett. 2001 Mar 1;76(2):139-44. doi: 10.1016/s0165-2478(01)00171-7.
Dietary copper deficiency impairs the function of both the vascular endothelium and circulating leukocytes. In the current study, leukocyte-endothelium adhesion was observed in the in vivo cremaster muscle microcirculation of copper-adequate and copper-deficient rats. Male, weanling Sprague-Dawley rats were fed purified diets that were either adequate (5.6 microg/g) or deficient (0.3 microg/g) in copper. Adhesion was stimulated with the inflammatory mediators tumor necrosis factor-alpha and bradykinin, and the chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine. Intravascular adhesion of leukocytes to the vascular endothelium was significantly attenuated in the copper-deficient group in response to all three agonists. These results occurred without any difference in intravascular wall shear rate between the dietary groups. Based on previous work, we propose that the attenuated response is caused by either decreased expression of adhesion molecules on leukocytes and endothelial cells or by inhibition of the endothelial cell calcium signaling associated with copper deficiency.
膳食铜缺乏会损害血管内皮细胞和循环白细胞的功能。在当前研究中，在铜充足和铜缺乏大鼠的体内提睾肌微循环中观察到白细胞与内皮细胞的黏附。将雄性断乳斯普拉格-道利大鼠喂食铜含量充足（5.6微克/克）或缺乏（0.3微克/克）的纯化饮食。用炎症介质肿瘤坏死因子-α、缓激肽和趋化肽N-甲酰甲硫氨酰-亮氨酰-苯丙氨酸刺激黏附。在所有三种激动剂作用下，铜缺乏组中白细胞与血管内皮细胞的血管内黏附显著减弱。这些结果出现时，各饮食组之间的血管内壁剪切率没有任何差异。基于之前的研究，我们提出这种减弱的反应是由白细胞和内皮细胞上黏附分子表达降低，或与铜缺乏相关的内皮细胞钙信号传导受抑制所致。
