A Molecular Study on Activation of Circulating Leukocytes in Metal-Induced Lung

本文研究了超细镍染毒大鼠白细胞和健康志愿者白细胞的活化作用。Ut-Ni组大鼠于灌胃Ut-Ni后7d，回收外周血白细胞，加入Ut-Ni培养。白细胞释放大量的NO和肿瘤坏死因子-α。在后者中，从健康志愿者身上回收外周血白细胞，并将其分离为单核细胞亚群和多形核亚群。用Ut-Ni、Ut-Co、Ut-Fe对两个亚群进行培养。UT-Ni诱导单核细胞释放IL-6、IL-8和TNF-α的作用最强。另一方面，Ut-Fe从单核细胞亚群产生的IL-1水平最高。UT-Ni不能从多核细胞亚群中释放细胞因子。综上所述，呼吸道接触Ut-Ni可引起外周血白细胞的激活。在人类中，如果外周单核细胞暴露于Ut-Ni，则可能随后激活。

Activation of leukocytes was studied in leukocytes from ultrafine-nickel instilled rat and in leukocytes from healthy volunteers. In the former, at seven days after rats were instilled with Ut-Ni, peripheral leukocytes were recovered and cultured with Ut-Ni. NO and tumor necrosis factor-alpha were highly released from leukocytes. In the latter, peripheral leukocytes recovered from healthy volunteers and separated into monocyte and polymorph nuclear subsets. The two subsets were cultured with Ut-Ni, Ut-Co, and Ut-Fe. Ut-Ni caused release interleukin 6 and 8, and TNF-alpha from the monocyte subset most highly among the three metals. On the other hand, Ut-Fe caused IL-1 most highly from the mononuclear subset. Ut-Ni did no release of cytokines from the polumorphonuclear subset. Taken together, respiratory exposure to Ut-Ni was suggested to cause activation of peripheral leukocytes. In human, if exposure to Ut-Ni of peripheral monocytes occur, activation may follow.