Yoshida Toshinori, Ohnuma Aya, Horiuchi Haruka, Harada Takanori
J Toxicol Pathol. 2011 Mar;24(1):9-24. doi: 10.1293/tox.24.9. Epub 2011 Mar 31.
Chronic lung injury resulting from a variety of different causes is frequently associated with the develop ment of pulmonary fibrosis in humans. Although the etiology of pulmonary fibrosis is generally unknown, several sources of evidence support the hypothesis that a number of environmental and occupational agents play an etiologic role in the pathogenesis of this disease. The agents discussed in this review include beryllium, nylon flock, textile printing aerosols, polyvinyl chloride and didecyldimethylammonium chloride. The authors also describe a variety of animal models, including genetically modified mice, in order to investigate the molecular mechanism of pulmonary fibrosis, focusing on chemokine receptors, regulatory T cells and transforming growth factor-β and bone morphogenetic protein signaling. Overall, we propose the concept of toxicological pulmonary fibrosis as a lung disease induced in response to environmental cues.
由多种不同原因导致的慢性肺损伤在人类中常与肺纤维化的发展相关。虽然肺纤维化的病因通常不明，但有若干证据来源支持这样一种假说，即许多环境和职业因素在该疾病的发病机制中起病因学作用。本综述中讨论的因素包括铍、尼龙绒毛、纺织印染气溶胶、聚氯乙烯和二癸基二甲基氯化铵。作者还描述了多种动物模型，包括基因改造小鼠，以便研究肺纤维化的分子机制，重点关注趋化因子受体、调节性T细胞以及转化生长因子-β和骨形态发生蛋白信号传导。总体而言，我们提出毒理学肺纤维化这一概念，将其作为一种因环境因素诱发的肺部疾病。
