Corsini E, Luster M I, Mahler J, Craig W A, Blazka M E, Rosenthal G J
Environmental Immunology and Neurobiology Section, National Institute of Environmental Health Sciences, Research Triange Park, North Carolina.
Am J Respir Cell Mol Biol. 1994 Nov;11(5):531-9. doi: 10.1165/ajrcmb.11.5.7946383.
Several lines of evidence have suggested that specific (i.e., lymphocyte) immunity plays a role in chemical-induced pulmonary diseases, including asbestosis. To evaluate the influence of cell-mediated immunity in pulmonary inflammation and fibrosis evoked by asbestos fibers, we compared the effects of asbestos in immunodeficient mice (Balb/c nu/nu and severe combined immunodeficient [C3H-SCID]), immunologically normal mice of the same genetic background, and immunodeficient mice reconstituted with syngeneic T lymphocytes. Increases in lavaged cell numbers occurred in asbestos-treated immunodeficient mice compared with asbestos-treated immunocompetent or immunodeficient mice that received T lymphocytes. Differential analysis of the collected cells in treated mice demonstrated a predominantly neutrophilic infiltrate that correlated with increased levels of leukotriene B4 and prostaglandin E2. There were no significant differences between immunocompetent and athymic asbestos-treated mice in bronchoalveolar lavaged total protein. However, asbestos-treated SCID mice revealed a significant increase in protein content and lactate dehydrogenase activity compared with asbestos-treated normal mice, which did not occur in T lymphocyte-reconstituted SCID mice. Fibronectin levels were elevated in asbestos-exposed athymic mice when compared with air-exposed athymic mice or asbestos-exposed immunocompetent mice. Both asbestos-treated athymic and SCID mice showed a significant increase in total lung hydroxyproline when compared with asbestos-treated immunocompetent mice. Lung hydroxyproline was also reduced in asbestos-exposed SCID mice after T lymphocyte reconstitution and, conversely, increased in T cell-depleted Balb/c mice.(ABSTRACT TRUNCATED AT 250 WORDS)
多项证据表明，特异性（即淋巴细胞）免疫在化学物质诱发的肺部疾病（包括石棉肺）中发挥作用。为了评估细胞介导的免疫在石棉纤维诱发的肺部炎症和纤维化中的影响，我们比较了石棉对免疫缺陷小鼠（Balb/c nu/nu和严重联合免疫缺陷 [C3H-SCID]）、相同遗传背景的免疫正常小鼠以及用同基因T淋巴细胞重建的免疫缺陷小鼠的影响。与接受T淋巴细胞的石棉处理的免疫 competent 或免疫缺陷小鼠相比，石棉处理的免疫缺陷小鼠的灌洗细胞数量增加。对处理过的小鼠中收集的细胞进行差异分析表明，主要是嗜中性粒细胞浸润，这与白三烯B4和前列腺素E2水平的增加相关。免疫 competent 和无胸腺石棉处理小鼠的支气管肺泡灌洗总蛋白之间没有显著差异。然而，与石棉处理的正常小鼠相比，石棉处理的SCID小鼠的蛋白含量和乳酸脱氢酶活性显著增加，而在T淋巴细胞重建的SCID小鼠中未出现这种情况。与空气暴露的无胸腺小鼠或石棉暴露的免疫 competent 小鼠相比，石棉暴露的无胸腺小鼠的纤连蛋白水平升高。与石棉处理的免疫 competent 小鼠相比，石棉处理的无胸腺和SCID小鼠的总肺羟脯氨酸均显著增加。T淋巴细胞重建后，石棉暴露的SCID小鼠的肺羟脯氨酸也降低，相反，T细胞耗竭的Balb/c小鼠的肺羟脯氨酸增加。（摘要截短于250字）
