Greene N D, Schneider S L
J Toxicol Environ Health. 1978 Sep-Nov;4(5-6):869-80. doi: 10.1080/15287397809529708.
Pulmonary alveolar macrophages (PAM) were obtained by lavage from baboons exposed for 6 mo to 2 ppm NO2 for 8 h/d, 5 d/wk, and the response of these cells to autologous migration inhibitory factor (MIF) was determined. PAM from two of three antigen-sensitized, NO2-exposed animals failed to respond to MIF derived from antigen-stimulated autologous lymphocytes. Similarly, PAM from three of the four NO2-exposed animals had diminished responsiveness to MIF obtained by phytohemagglutinin stimulation of their own lymphocytes. The altered responsiveness resulted from an effect on the macrophages and not on the lymphocytes used to prepare the MIF, as shown by the normal blastogenic responsiveness of the lymphocytes and the normal activity of the MIF thus produced on guinea pig peritoneal macrophages. These results demonstrate that inhalation of 2 ppm NO2 may have important subtle effects on pulmonary cells, which may result in altered immune capabilities within the lung.
通过对狒狒进行灌洗获取肺泡巨噬细胞（PAM），这些狒狒每天暴露于2 ppm二氧化氮8小时，每周5天，持续6个月。测定了这些细胞对自体迁移抑制因子（MIF）的反应。三只经抗原致敏且暴露于二氧化氮的动物中，有两只的PAM对源自抗原刺激的自体淋巴细胞的MIF无反应。同样，四只暴露于二氧化氮的动物中有三只的PAM对通过植物血凝素刺激其自身淋巴细胞获得的MIF反应性降低。淋巴细胞的正常增殖反应性以及由此产生的MIF对豚鼠腹腔巨噬细胞的正常活性表明，反应性改变是对巨噬细胞的影响，而非对用于制备MIF的淋巴细胞的影响。这些结果表明，吸入2 ppm二氧化氮可能对肺细胞产生重要的细微影响，这可能导致肺内免疫能力改变。
