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

研究了灌注超细镍的大鼠白细胞和健康志愿者白细胞的活化情况。前者，在大鼠输注Ut-Ni后7天，外周血白细胞恢复并用Ut-Ni培养。NO和肿瘤坏死因子- α从白细胞中大量释放。在后者中，外周白细胞从健康志愿者中恢复并分离成单核细胞和多态核亚群。这两个亚群分别用Ut-Ni、Ut-Co和Ut-Fe培养。在三种金属中，Ut-Ni引起单核细胞亚群释放白细胞介素6、8和tnf - α的程度最高。另一方面，Ut-Fe对IL-1的影响主要来自单核亚群。Ut-Ni不释放多形核亚群的细胞因子。综上所述，呼吸道暴露于Ut-Ni可能会引起外周白细胞的激活。在人类，如果暴露于Ut-Ni外周单核细胞发生，激活可能随之而来。

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.