二氧化硅和粉煤灰粉尘吸入对肺泡巨噬细胞效应细胞功能的影响。

C A Burns, A Zarkower
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摘要

研究发现,吸入二氧化硅在暴露14、42和70天后会显著增强肺泡巨噬细胞抗体依赖细胞介导的细胞毒性(ADCC),而使用粉煤灰的类似处理在暴露42天后会显著抑制ADCC。吸入二氧化硅和粉煤灰均可抑制bcg激发和bcg再激发动物肺泡巨噬细胞介导肿瘤细胞裂解的能力。粉煤灰暴露也显著抑制了bcg激活的巨噬细胞通过ADCC机制裂解靶细胞的能力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The effects of silica and fly ash dust inhalation on alveolar macrophage effector cell function.

Inhalation of silica was found to cause significant enhancement of alveolar macrophage antibody-dependent cell-mediated cytotoxicity (ADCC) after 14, 42, and 70 days of exposure, while similar treatment using fly ash resulted in significant suppression of ADCC after 42 days of exposure. Both silica and fly ash inhalation depressed the ability of alveolar macrophages from BCG-primed and BCG-rechallenged animals to mediate tumor cell lysis. Fly ash exposure also significantly suppressed the ability of BCG-activated macrophages to lyse target cells by the ADCC mechanism.

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