Brody A R
Scan Electron Microsc. 1984(Pt 1):167-71.
This paper presents new findings obtained using animal models on the basic mechanisms of asbestos-induced lung disease. Recent, highly visible reviews on the subject have clearly pointed out that little is known about the cellular mechanisms through which inhaled asbestos fibers cause the well known, debilitating lung disease - asbestosis (i.e. interstitial pulmonary fibrosis). During the past five years, my colleagues and I have published a series of papers in which we have attempted to elucidate, in a rat model of asbestosis, the initial events of 1) asbestos fiber deposition, 2) translocation of fibers to the lung interstitium, 3) the response of pulmonary macrophages and the mechanisms through which these cells are attracted to sites of initial asbestos deposition, and 4) the developmental pathogenesis of the earliest anatomic lesion consequent to asbestos exposure.
本文介绍了利用动物模型在石棉诱导的肺部疾病基本机制方面获得的新发现。近期关于该主题的一些备受瞩目的综述明确指出，对于吸入的石棉纤维导致众所周知的、使人衰弱的肺部疾病——石棉沉着病（即间质性肺纤维化）的细胞机制，我们了解甚少。在过去五年中，我和我的同事发表了一系列论文，在石棉沉着病大鼠模型中试图阐明以下初始事件：1）石棉纤维沉积；2）纤维向肺间质的转运；3）肺巨噬细胞的反应以及这些细胞被吸引至石棉初始沉积部位的机制；4）石棉暴露后最早解剖学病变的发育发病机制。
